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trim55 antibody  (Thermo Fisher)


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    Thermo Fisher trim55 antibody
    <t>Trim55</t> Expression Was Significantly Increased After MI (A, B) Quantification and representative images of Western blot analyses showing Trim55 protein expression in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (C) Quantification of Trim55 mRNA levels in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (D, E) Quantification and representative images of Trim55 immunohistochemistry in the border zone of myocardium at 3 and 28 days after MI (n = 3; scale bar: 50 μm). (F, G) Quantification and representative images of Western blot analyses showing Trim55 protein expression in NRCM cells after 400 μmol/L stimulation at 24 hours (n = 3). (H) Quantification of Trim55 mRNA levels in NRCM cells after CoCl 2 stimulation (400 μmol/L; 24 hours; n = 3). All data are expressed as mean ± SEM. Data in B, C, E, G, and H were analyzed using Student’s t -test. ∗ P < 0.05, ∗∗ P < 0.01 vs the control or sham group. CoCl 2 = cobalt chloride; CON = control; GADPH = glyceraldehyde-3-phosphate dehydrogenase; IHC = immunohistochemistry; MI = myocardial infarction; mRNA = messenger RNA; NRCM = neonatal rat cardiomyocyte; Trim55 = tripartite motif-containing 55.
    Trim55 Antibody, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/trim55+antibody/pmc11494394-52-39-41?v=Thermo+Fisher
    Average 90 stars, based on 1 article reviews
    trim55 antibody - by Bioz Stars, 2026-07
    90/100 stars

    Images

    1) Product Images from "TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway"

    Article Title: TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway

    Journal: JACC: Basic to Translational Science

    doi: 10.1016/j.jacbts.2024.05.006

    Trim55 Expression Was Significantly Increased After MI (A, B) Quantification and representative images of Western blot analyses showing Trim55 protein expression in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (C) Quantification of Trim55 mRNA levels in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (D, E) Quantification and representative images of Trim55 immunohistochemistry in the border zone of myocardium at 3 and 28 days after MI (n = 3; scale bar: 50 μm). (F, G) Quantification and representative images of Western blot analyses showing Trim55 protein expression in NRCM cells after 400 μmol/L stimulation at 24 hours (n = 3). (H) Quantification of Trim55 mRNA levels in NRCM cells after CoCl 2 stimulation (400 μmol/L; 24 hours; n = 3). All data are expressed as mean ± SEM. Data in B, C, E, G, and H were analyzed using Student’s t -test. ∗ P < 0.05, ∗∗ P < 0.01 vs the control or sham group. CoCl 2 = cobalt chloride; CON = control; GADPH = glyceraldehyde-3-phosphate dehydrogenase; IHC = immunohistochemistry; MI = myocardial infarction; mRNA = messenger RNA; NRCM = neonatal rat cardiomyocyte; Trim55 = tripartite motif-containing 55.
    Figure Legend Snippet: Trim55 Expression Was Significantly Increased After MI (A, B) Quantification and representative images of Western blot analyses showing Trim55 protein expression in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (C) Quantification of Trim55 mRNA levels in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (D, E) Quantification and representative images of Trim55 immunohistochemistry in the border zone of myocardium at 3 and 28 days after MI (n = 3; scale bar: 50 μm). (F, G) Quantification and representative images of Western blot analyses showing Trim55 protein expression in NRCM cells after 400 μmol/L stimulation at 24 hours (n = 3). (H) Quantification of Trim55 mRNA levels in NRCM cells after CoCl 2 stimulation (400 μmol/L; 24 hours; n = 3). All data are expressed as mean ± SEM. Data in B, C, E, G, and H were analyzed using Student’s t -test. ∗ P < 0.05, ∗∗ P < 0.01 vs the control or sham group. CoCl 2 = cobalt chloride; CON = control; GADPH = glyceraldehyde-3-phosphate dehydrogenase; IHC = immunohistochemistry; MI = myocardial infarction; mRNA = messenger RNA; NRCM = neonatal rat cardiomyocyte; Trim55 = tripartite motif-containing 55.

    Techniques Used: Expressing, Western Blot, Immunohistochemistry, Control

    Trim55 Knockout Alleviated Myocardial Injury and Cardiomyocyte Apoptosis After MI (A) Echocardiographic analysis of the LVEF and FS at 28 days after MI in the C57-sham (n = 10), Trim55 –/– -sham (n = 10), C57-MI (n = 10), and Trim55 –/– -MI (n = 10) groups. (B) Quantitative analysis of the ratio of heart weight to body weight at 28 days after MI in the C57-sham (n = 10), Trim55 –/– -sham (n = 10), C57-MI (n = 8), and Trim55 –/– -MI (n = 10) groups. (C, D) Representative HE and Masson staining pictures and quantification of the infarction area at 28 days after MI in the C57-sham, Trim55 –/– -sham, C57-MI, and Trim55 –/– -MI groups (n = 3). (E, F) Quantification and representative images of Western blot analyses showing the Trim55, collagen I, and TGF-β protein expression in the C57-sham, Trim55 –/– -sham, C57-MI, and Trim55 –/– -MI groups (n = 3). (G, H) Quantification and representative images of Western blot analyses showing the Trim55, Bax, Bcl2, cleaved caspase-3, and cleaved caspase-8 protein expression in the C57-sham (n = 3), Trim55 –/– -sham (n = 3), C57-MI (n = 4), and Trim55 –/– -MI (n = 3) groups. (I, J) Representative TUNEL staining images and quantification of apoptotic positive cells at 3 days after MI in the C57-sham (n = 3), Trim55 –/– -sham (n = 3), C57-MI (n = 3), and Trim55 –/– -MI (n = 4) groups. All data in A, B, D, F, H, and J are expressed as mean ± SEM. Data in A, B, D, F, H, and J were analyzed using 2-way analysis of variance followed by the Bonferroni post hoc test. ∗∗ P < 0.01 vs C57-sham; † P < 0.05 vs Trim55 –/– -sham; ‡ P < 0.05 vs C57-MI. Bax = BCL2 associated X apoptosis regulator; Bcl-2 = BCL2 apoptosis regulator; BW = body weight; FS = fraction shortening; HE = hematoxylin and eosin; HW = heart weight; LVEF = left ventricular ejection fraction; TGF = transforming growth factor; TUNEL = terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling; other abbreviations as in <xref ref-type=Figure 1 . " title="Trim55 Knockout Alleviated Myocardial Injury and Cardiomyocyte Apoptosis After ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Trim55 Knockout Alleviated Myocardial Injury and Cardiomyocyte Apoptosis After MI (A) Echocardiographic analysis of the LVEF and FS at 28 days after MI in the C57-sham (n = 10), Trim55 –/– -sham (n = 10), C57-MI (n = 10), and Trim55 –/– -MI (n = 10) groups. (B) Quantitative analysis of the ratio of heart weight to body weight at 28 days after MI in the C57-sham (n = 10), Trim55 –/– -sham (n = 10), C57-MI (n = 8), and Trim55 –/– -MI (n = 10) groups. (C, D) Representative HE and Masson staining pictures and quantification of the infarction area at 28 days after MI in the C57-sham, Trim55 –/– -sham, C57-MI, and Trim55 –/– -MI groups (n = 3). (E, F) Quantification and representative images of Western blot analyses showing the Trim55, collagen I, and TGF-β protein expression in the C57-sham, Trim55 –/– -sham, C57-MI, and Trim55 –/– -MI groups (n = 3). (G, H) Quantification and representative images of Western blot analyses showing the Trim55, Bax, Bcl2, cleaved caspase-3, and cleaved caspase-8 protein expression in the C57-sham (n = 3), Trim55 –/– -sham (n = 3), C57-MI (n = 4), and Trim55 –/– -MI (n = 3) groups. (I, J) Representative TUNEL staining images and quantification of apoptotic positive cells at 3 days after MI in the C57-sham (n = 3), Trim55 –/– -sham (n = 3), C57-MI (n = 3), and Trim55 –/– -MI (n = 4) groups. All data in A, B, D, F, H, and J are expressed as mean ± SEM. Data in A, B, D, F, H, and J were analyzed using 2-way analysis of variance followed by the Bonferroni post hoc test. ∗∗ P < 0.01 vs C57-sham; † P < 0.05 vs Trim55 –/– -sham; ‡ P < 0.05 vs C57-MI. Bax = BCL2 associated X apoptosis regulator; Bcl-2 = BCL2 apoptosis regulator; BW = body weight; FS = fraction shortening; HE = hematoxylin and eosin; HW = heart weight; LVEF = left ventricular ejection fraction; TGF = transforming growth factor; TUNEL = terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling; other abbreviations as in Figure 1 .

    Techniques Used: Knock-Out, Staining, Western Blot, Expressing, TUNEL Assay, End Labeling

    Trim55 Overexpression Promoted Cardiomyocyte Apoptosis Induced by Hypoxia (A, B) Quantification and representative images of Western blots showing the expression of apoptosis-related proteins after Trim55 overexpression (n = 3). (C, D) Effects of Trim55 overexpression and CoCl treatment on the expression of apoptosis-related proteins by Western blot (n = 3). (E, F) Effects of Trim55 overexpression and CoCl treatment on cardiomyocyte apoptosis by flow cytometry analysis (n = 4). (G, H) Effects of Trim55 overexpression and CoCl treatment on cardiomyocyte apoptosis by TUNEL staining (n = 3). CoCl : 400 μmol/L, 24 hours. All data in B, D, F, and H are expressed as mean ± SEM. Data in B were analyzed using an unpaired Student’s t -test. Data in D, F, and H were analyzed using 2-way analysis of variance followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon; † P < 0.05 vs adTrim55; ‡ P < 0.05 vs adcon + CoCl . adcon = adenovirus control; adTrim55 = Trim55-overexpressing adenovirus; DAPI = 4′,6-diamidino-2-phenylindole; ns = not significant; other abbreviations as in <xref ref-type=Figures 1 and . " title="Trim55 Overexpression Promoted Cardiomyocyte Apoptosis Induced by Hypoxia (A, ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Trim55 Overexpression Promoted Cardiomyocyte Apoptosis Induced by Hypoxia (A, B) Quantification and representative images of Western blots showing the expression of apoptosis-related proteins after Trim55 overexpression (n = 3). (C, D) Effects of Trim55 overexpression and CoCl treatment on the expression of apoptosis-related proteins by Western blot (n = 3). (E, F) Effects of Trim55 overexpression and CoCl treatment on cardiomyocyte apoptosis by flow cytometry analysis (n = 4). (G, H) Effects of Trim55 overexpression and CoCl treatment on cardiomyocyte apoptosis by TUNEL staining (n = 3). CoCl : 400 μmol/L, 24 hours. All data in B, D, F, and H are expressed as mean ± SEM. Data in B were analyzed using an unpaired Student’s t -test. Data in D, F, and H were analyzed using 2-way analysis of variance followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon; † P < 0.05 vs adTrim55; ‡ P < 0.05 vs adcon + CoCl . adcon = adenovirus control; adTrim55 = Trim55-overexpressing adenovirus; DAPI = 4′,6-diamidino-2-phenylindole; ns = not significant; other abbreviations as in Figures 1 and .

    Techniques Used: Over Expression, Western Blot, Expressing, Flow Cytometry, TUNEL Assay, Staining, Control

    Trim55 Knockdown Alleviated Cardiomyocyte Apoptosis Induced by Hypoxia (A, B) Quantification and representative images of Western blot analyses showing the expression of apoptosis-related proteins after Trim55 knockdown (n = 3). (C, D) Effects of Trim55 knockdown and CoCl 2 treatment on the expression of apoptosis-related proteins by Western blot (n = 3). (E, F) Effects of Trim55 knockout and CoCl 2 treatment on cardiomyocyte apoptosis by flow cytometry analysis (n = 4). (G, H) Effects of Trim55 knockdown and CoCl 2 treatment on cardiomyocyte apoptosis by TUNEL staining (n = 3). All data in B, D, F, and H are expressed as mean ± SEM. Data in B were analyzed using an unpaired Student’s t -test. Data in D, F, and H were analyzed using 2-way analysis of variance, followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs si-nc; ‡ P < 0.05 vs si-Trim55; † P < 0.05 vs si-nc + CoCl 2 . si-nc = siRNA-normal control; si-Trim55 = Trim55-interfering RNA; other abbreviations as in <xref ref-type=Figure 1 , Figure 2 , Figure 3 . " title="Trim55 Knockdown Alleviated Cardiomyocyte Apoptosis Induced by Hypoxia (A, ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Trim55 Knockdown Alleviated Cardiomyocyte Apoptosis Induced by Hypoxia (A, B) Quantification and representative images of Western blot analyses showing the expression of apoptosis-related proteins after Trim55 knockdown (n = 3). (C, D) Effects of Trim55 knockdown and CoCl 2 treatment on the expression of apoptosis-related proteins by Western blot (n = 3). (E, F) Effects of Trim55 knockout and CoCl 2 treatment on cardiomyocyte apoptosis by flow cytometry analysis (n = 4). (G, H) Effects of Trim55 knockdown and CoCl 2 treatment on cardiomyocyte apoptosis by TUNEL staining (n = 3). All data in B, D, F, and H are expressed as mean ± SEM. Data in B were analyzed using an unpaired Student’s t -test. Data in D, F, and H were analyzed using 2-way analysis of variance, followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs si-nc; ‡ P < 0.05 vs si-Trim55; † P < 0.05 vs si-nc + CoCl 2 . si-nc = siRNA-normal control; si-Trim55 = Trim55-interfering RNA; other abbreviations as in Figure 1 , Figure 2 , Figure 3 .

    Techniques Used: Knockdown, Western Blot, Expressing, Knock-Out, Flow Cytometry, TUNEL Assay, Staining, Control

    Trim55 Promoted Oxidative Stress by Inhibiting the Nrf2/HO-1 Pathway in Cardiomyocytes (A) Quantification and representative images of Western blot analyses showing the expression of antioxidant proteins (P62, Nrf2, HO-1) after overexpression of Trim55 in cardiomyocytes (n = 3). (B) Quantification and representative images of Western blot analyses showing the expression of antioxidant proteins (P62, Nrf2, HO-1) after Trim55 knockdown (n = 3). (C) Effects of Trim55 overexpression on the intracellular ROS levels by flow cytometry (n = 5). (D) Effects of Trim55 silencing on the intracellular ROS levels by flow cytometry (n = 5). (E) Quantification and representative images of CellROX staining after Trim55 overexpression (n = 3). (F) Quantification and representative images of CellROX staining after Trim55 knockdown (n = 3). All data in A to F are expressed as mean ±SEM. Data in A to F were analyzed by Student’s t -test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon or si-nc. APC = allophycocyanin; HO-1 = heme oxygenase 1; ISO = isotype control; Nrf2 = nuclear factor, erythroid derived 2; ROS = reactive oxygen species; other abbreviations as in <xref ref-type=Figure 1 , Figure 2 , Figure 3 , Figure 4 . " title="Trim55 Promoted Oxidative Stress by Inhibiting the Nrf2/HO-1 Pathway ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Trim55 Promoted Oxidative Stress by Inhibiting the Nrf2/HO-1 Pathway in Cardiomyocytes (A) Quantification and representative images of Western blot analyses showing the expression of antioxidant proteins (P62, Nrf2, HO-1) after overexpression of Trim55 in cardiomyocytes (n = 3). (B) Quantification and representative images of Western blot analyses showing the expression of antioxidant proteins (P62, Nrf2, HO-1) after Trim55 knockdown (n = 3). (C) Effects of Trim55 overexpression on the intracellular ROS levels by flow cytometry (n = 5). (D) Effects of Trim55 silencing on the intracellular ROS levels by flow cytometry (n = 5). (E) Quantification and representative images of CellROX staining after Trim55 overexpression (n = 3). (F) Quantification and representative images of CellROX staining after Trim55 knockdown (n = 3). All data in A to F are expressed as mean ±SEM. Data in A to F were analyzed by Student’s t -test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon or si-nc. APC = allophycocyanin; HO-1 = heme oxygenase 1; ISO = isotype control; Nrf2 = nuclear factor, erythroid derived 2; ROS = reactive oxygen species; other abbreviations as in Figure 1 , Figure 2 , Figure 3 , Figure 4 .

    Techniques Used: Western Blot, Expressing, Over Expression, Knockdown, Flow Cytometry, Staining, Control, Derivative Assay

    Trim55 Promoted Cardiomyocyte Apoptosis Through Inhibiting the Nrf2/HO-1 Signaling Pathway (A) Effects of Trim55 overexpression and HO-1 overexpression on the expression of Trim55, HO-1, cleaved caspase-3, and cleaved caspase-8 by Western blot (n = 3). (B) Effects of Trim55 overexpression and HO-1 overexpression on cardiomyocyte apoptosis by flow cytometry (n = 4). (C) Effects of Trim55 overexpression and HO-1 overexpression on cardiomyocyte apoptosis by TUNEL staining (n = 3). (D) Effects of Trim55 knockdown and HO-1 knockdown on the expressions of cleaved caspase-3 and cleaved caspase-8 by Western blot (n = 3). (E) Effects of Trim55 knockdown and HO-1 knockdown on cardiomyocyte apoptosis by flow cytometry (n = 4). (F) Effects of Trim55 knockdown and HO-1 knockdown on cardiomyocyte apoptosis by TUNEL staining (n = 3). All data in A to F are expressed as mean ± SEM. Data in A to F were analyzed by 2-way analysis of variance followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon or si-nc; † P < 0.05 vs adTrim55 or si-nc + si HO-1; ‡ P < 0.05 vs adcon + pcDNA3.1 HO-1 or si-Trim55. Abbreviations as in <xref ref-type=Figure 1 , Figure 2 , Figure 3 , Figure 4 , Figure 5 . " title="Trim55 Promoted Cardiomyocyte Apoptosis Through Inhibiting the Nrf2/HO-1 Signaling ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Trim55 Promoted Cardiomyocyte Apoptosis Through Inhibiting the Nrf2/HO-1 Signaling Pathway (A) Effects of Trim55 overexpression and HO-1 overexpression on the expression of Trim55, HO-1, cleaved caspase-3, and cleaved caspase-8 by Western blot (n = 3). (B) Effects of Trim55 overexpression and HO-1 overexpression on cardiomyocyte apoptosis by flow cytometry (n = 4). (C) Effects of Trim55 overexpression and HO-1 overexpression on cardiomyocyte apoptosis by TUNEL staining (n = 3). (D) Effects of Trim55 knockdown and HO-1 knockdown on the expressions of cleaved caspase-3 and cleaved caspase-8 by Western blot (n = 3). (E) Effects of Trim55 knockdown and HO-1 knockdown on cardiomyocyte apoptosis by flow cytometry (n = 4). (F) Effects of Trim55 knockdown and HO-1 knockdown on cardiomyocyte apoptosis by TUNEL staining (n = 3). All data in A to F are expressed as mean ± SEM. Data in A to F were analyzed by 2-way analysis of variance followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon or si-nc; † P < 0.05 vs adTrim55 or si-nc + si HO-1; ‡ P < 0.05 vs adcon + pcDNA3.1 HO-1 or si-Trim55. Abbreviations as in Figure 1 , Figure 2 , Figure 3 , Figure 4 , Figure 5 .

    Techniques Used: Over Expression, Expressing, Western Blot, Flow Cytometry, TUNEL Assay, Staining, Knockdown

    Foxo3 Was a Direct Upstream Transcription Factor of Trim55 (A, B) Quantification and representative images of Western blots showing the expression of Foxo3, Gata3, Hoxa5, and Stat3 after CoCl 2 hypoxia in NRCMs (n = 3). ∗ P < 0.05 vs CON. (C, D) Foxo3 expression in the myocardium post-MI. (n = 3). ∗ P < 0.05, ∗∗ P < 0.01 vs sham (E, F) Quantification and representative images of Western blot analyses showing the expression of Trim55 after Foxo3 overexpression in NRCMs (n = 3). ∗∗ P < 0.01 vs CON. (G) Quantification of Trim55 mRNA levels in NRCMs after Foxo3 overexpression (n = 3). ∗∗ P < 0.01 vs CON. (H, I) Quantification and representative images of Western blot analyses showing the expression of Trim55 after knockdown in NRCMs (n = 3). † P < 0.05 vs si-nc. (J) Quantification of Trim55 mRNA levels in NRCMs after Foxo3 knockdown (n = 3). † P < 0.05 vs si-nc. (K) Possible binding sites of Foxo3 and Trim55 were predicted using the JASPAR website. (L) Relative luciferase activity in HEK293T cells with cotransfection with Foxo3-overexpressing plasmid and with WT-Trim55 plasmid or Mut-Trim55 plasmid. ∗∗ P < 0.01 vs NC Foxo3 + WT-Trim55; ‡ P < 0.05 vs NC Foxo3 + Mut-Trim55 (n = 12). (M) The effect of Trim55 on cardiomyocyte apoptosis after MI (by Figdraw). All data in B, D, F, G, H, and J are expressed as mean ± SEM. Data in B, D, F, G, and H were analyzed using Student’s t -test. Data in J were analyzed using 2-way analysis of variance, followed by the Bonferroni post hoc test. Foxo3 = forkhead box transcription factor 3; Mut = mutated; NC = normal control; WT = wild type; other abbreviations as in <xref ref-type=Figure 1 , Figure 2 , Figure 3 , Figure 4 , Figure 5 . " title="Foxo3 Was a Direct Upstream Transcription Factor of Trim55 (A, B) Quantification and representative images of Western ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Foxo3 Was a Direct Upstream Transcription Factor of Trim55 (A, B) Quantification and representative images of Western blots showing the expression of Foxo3, Gata3, Hoxa5, and Stat3 after CoCl 2 hypoxia in NRCMs (n = 3). ∗ P < 0.05 vs CON. (C, D) Foxo3 expression in the myocardium post-MI. (n = 3). ∗ P < 0.05, ∗∗ P < 0.01 vs sham (E, F) Quantification and representative images of Western blot analyses showing the expression of Trim55 after Foxo3 overexpression in NRCMs (n = 3). ∗∗ P < 0.01 vs CON. (G) Quantification of Trim55 mRNA levels in NRCMs after Foxo3 overexpression (n = 3). ∗∗ P < 0.01 vs CON. (H, I) Quantification and representative images of Western blot analyses showing the expression of Trim55 after knockdown in NRCMs (n = 3). † P < 0.05 vs si-nc. (J) Quantification of Trim55 mRNA levels in NRCMs after Foxo3 knockdown (n = 3). † P < 0.05 vs si-nc. (K) Possible binding sites of Foxo3 and Trim55 were predicted using the JASPAR website. (L) Relative luciferase activity in HEK293T cells with cotransfection with Foxo3-overexpressing plasmid and with WT-Trim55 plasmid or Mut-Trim55 plasmid. ∗∗ P < 0.01 vs NC Foxo3 + WT-Trim55; ‡ P < 0.05 vs NC Foxo3 + Mut-Trim55 (n = 12). (M) The effect of Trim55 on cardiomyocyte apoptosis after MI (by Figdraw). All data in B, D, F, G, H, and J are expressed as mean ± SEM. Data in B, D, F, G, and H were analyzed using Student’s t -test. Data in J were analyzed using 2-way analysis of variance, followed by the Bonferroni post hoc test. Foxo3 = forkhead box transcription factor 3; Mut = mutated; NC = normal control; WT = wild type; other abbreviations as in Figure 1 , Figure 2 , Figure 3 , Figure 4 , Figure 5 .

    Techniques Used: Western Blot, Expressing, Over Expression, Knockdown, Binding Assay, Luciferase, Activity Assay, Cotransfection, Plasmid Preparation, Control



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    Novus Biologicals human trim55 antibody
    Figure 1. <t>TRIM55</t> is downregulated in HCC tissues and is associated with prognosis of HCC patients. (A) IHC detected expression of TRIM55 in HCC tissues and neighboring tissues. Representative photos at 200× and 400×. The level of TRIM55 expression between HCC tissues and neighbor tissues was analyzed and shown as a pie chart. (B, C) the relationship between overall survival and TRIM55 expression was analyzed by Kaplan-Meier analysis, and the follow-up data were collected by ourselves (B) or TCGA database (C).
    Human Trim55 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/trim55+antibody/10__12659_slash_msm__910984-38-16-19?v=Novus+Biologicals
    Average 90 stars, based on 1 article reviews
    human trim55 antibody - by Bioz Stars, 2026-07
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    Aviva Systems murf2
    Fig. 1 MuRF1 and <t>MuRF2</t> are highly induced during skeletal muscle regeneration. (a) MuRF1, MuRF2 and Mafbx/Atrogin‐1 immunoblots 3 and 10 days after TA CTX injury. Sarcomeric actin is a loading control. (b‐g) Immunolocalization of MuRF1 and (j‐o) MuRF2, 3 and 10 days after CTX injury in TA muscle. In h‐i and p‐q, primary antibodies were not used in the assay. Immunodetection of laminin (green) was used to outline muscle fibers. (h‐i and p‐q) No primary antibodies were added to the assay. Images were obtained with a fluorescence microscope and a 40x air medium objective. Bar, 50µm
    Murf2, supplied by Aviva Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/trim55+antibody/10__1002_slash_j__2617___1619__2019__tb00010__x-63-11-38?v=Aviva+Systems
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    Image Search Results


    Trim55 Expression Was Significantly Increased After MI (A, B) Quantification and representative images of Western blot analyses showing Trim55 protein expression in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (C) Quantification of Trim55 mRNA levels in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (D, E) Quantification and representative images of Trim55 immunohistochemistry in the border zone of myocardium at 3 and 28 days after MI (n = 3; scale bar: 50 μm). (F, G) Quantification and representative images of Western blot analyses showing Trim55 protein expression in NRCM cells after 400 μmol/L stimulation at 24 hours (n = 3). (H) Quantification of Trim55 mRNA levels in NRCM cells after CoCl 2 stimulation (400 μmol/L; 24 hours; n = 3). All data are expressed as mean ± SEM. Data in B, C, E, G, and H were analyzed using Student’s t -test. ∗ P < 0.05, ∗∗ P < 0.01 vs the control or sham group. CoCl 2 = cobalt chloride; CON = control; GADPH = glyceraldehyde-3-phosphate dehydrogenase; IHC = immunohistochemistry; MI = myocardial infarction; mRNA = messenger RNA; NRCM = neonatal rat cardiomyocyte; Trim55 = tripartite motif-containing 55.

    Journal: JACC: Basic to Translational Science

    Article Title: TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway

    doi: 10.1016/j.jacbts.2024.05.006

    Figure Lengend Snippet: Trim55 Expression Was Significantly Increased After MI (A, B) Quantification and representative images of Western blot analyses showing Trim55 protein expression in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (C) Quantification of Trim55 mRNA levels in the border zone of myocardium at 3, 7, and 28 days after MI (n = 3). (D, E) Quantification and representative images of Trim55 immunohistochemistry in the border zone of myocardium at 3 and 28 days after MI (n = 3; scale bar: 50 μm). (F, G) Quantification and representative images of Western blot analyses showing Trim55 protein expression in NRCM cells after 400 μmol/L stimulation at 24 hours (n = 3). (H) Quantification of Trim55 mRNA levels in NRCM cells after CoCl 2 stimulation (400 μmol/L; 24 hours; n = 3). All data are expressed as mean ± SEM. Data in B, C, E, G, and H were analyzed using Student’s t -test. ∗ P < 0.05, ∗∗ P < 0.01 vs the control or sham group. CoCl 2 = cobalt chloride; CON = control; GADPH = glyceraldehyde-3-phosphate dehydrogenase; IHC = immunohistochemistry; MI = myocardial infarction; mRNA = messenger RNA; NRCM = neonatal rat cardiomyocyte; Trim55 = tripartite motif-containing 55.

    Article Snippet: After rehydration in citrate buffer solution and a 40-minute antigen recovery process, mouse heart slices were permeabilized with 0.2% Triton X-100 in PBS for 15 minutes, sealed with 5% bovine serum albumin for 1 hour, and stained overnight with Trim55 (1:50, Thermo Fisher Scientific) antibody.

    Techniques: Expressing, Western Blot, Immunohistochemistry, Control

    Trim55 Knockout Alleviated Myocardial Injury and Cardiomyocyte Apoptosis After MI (A) Echocardiographic analysis of the LVEF and FS at 28 days after MI in the C57-sham (n = 10), Trim55 –/– -sham (n = 10), C57-MI (n = 10), and Trim55 –/– -MI (n = 10) groups. (B) Quantitative analysis of the ratio of heart weight to body weight at 28 days after MI in the C57-sham (n = 10), Trim55 –/– -sham (n = 10), C57-MI (n = 8), and Trim55 –/– -MI (n = 10) groups. (C, D) Representative HE and Masson staining pictures and quantification of the infarction area at 28 days after MI in the C57-sham, Trim55 –/– -sham, C57-MI, and Trim55 –/– -MI groups (n = 3). (E, F) Quantification and representative images of Western blot analyses showing the Trim55, collagen I, and TGF-β protein expression in the C57-sham, Trim55 –/– -sham, C57-MI, and Trim55 –/– -MI groups (n = 3). (G, H) Quantification and representative images of Western blot analyses showing the Trim55, Bax, Bcl2, cleaved caspase-3, and cleaved caspase-8 protein expression in the C57-sham (n = 3), Trim55 –/– -sham (n = 3), C57-MI (n = 4), and Trim55 –/– -MI (n = 3) groups. (I, J) Representative TUNEL staining images and quantification of apoptotic positive cells at 3 days after MI in the C57-sham (n = 3), Trim55 –/– -sham (n = 3), C57-MI (n = 3), and Trim55 –/– -MI (n = 4) groups. All data in A, B, D, F, H, and J are expressed as mean ± SEM. Data in A, B, D, F, H, and J were analyzed using 2-way analysis of variance followed by the Bonferroni post hoc test. ∗∗ P < 0.01 vs C57-sham; † P < 0.05 vs Trim55 –/– -sham; ‡ P < 0.05 vs C57-MI. Bax = BCL2 associated X apoptosis regulator; Bcl-2 = BCL2 apoptosis regulator; BW = body weight; FS = fraction shortening; HE = hematoxylin and eosin; HW = heart weight; LVEF = left ventricular ejection fraction; TGF = transforming growth factor; TUNEL = terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling; other abbreviations as in <xref ref-type=Figure 1 . " width="100%" height="100%">

    Journal: JACC: Basic to Translational Science

    Article Title: TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway

    doi: 10.1016/j.jacbts.2024.05.006

    Figure Lengend Snippet: Trim55 Knockout Alleviated Myocardial Injury and Cardiomyocyte Apoptosis After MI (A) Echocardiographic analysis of the LVEF and FS at 28 days after MI in the C57-sham (n = 10), Trim55 –/– -sham (n = 10), C57-MI (n = 10), and Trim55 –/– -MI (n = 10) groups. (B) Quantitative analysis of the ratio of heart weight to body weight at 28 days after MI in the C57-sham (n = 10), Trim55 –/– -sham (n = 10), C57-MI (n = 8), and Trim55 –/– -MI (n = 10) groups. (C, D) Representative HE and Masson staining pictures and quantification of the infarction area at 28 days after MI in the C57-sham, Trim55 –/– -sham, C57-MI, and Trim55 –/– -MI groups (n = 3). (E, F) Quantification and representative images of Western blot analyses showing the Trim55, collagen I, and TGF-β protein expression in the C57-sham, Trim55 –/– -sham, C57-MI, and Trim55 –/– -MI groups (n = 3). (G, H) Quantification and representative images of Western blot analyses showing the Trim55, Bax, Bcl2, cleaved caspase-3, and cleaved caspase-8 protein expression in the C57-sham (n = 3), Trim55 –/– -sham (n = 3), C57-MI (n = 4), and Trim55 –/– -MI (n = 3) groups. (I, J) Representative TUNEL staining images and quantification of apoptotic positive cells at 3 days after MI in the C57-sham (n = 3), Trim55 –/– -sham (n = 3), C57-MI (n = 3), and Trim55 –/– -MI (n = 4) groups. All data in A, B, D, F, H, and J are expressed as mean ± SEM. Data in A, B, D, F, H, and J were analyzed using 2-way analysis of variance followed by the Bonferroni post hoc test. ∗∗ P < 0.01 vs C57-sham; † P < 0.05 vs Trim55 –/– -sham; ‡ P < 0.05 vs C57-MI. Bax = BCL2 associated X apoptosis regulator; Bcl-2 = BCL2 apoptosis regulator; BW = body weight; FS = fraction shortening; HE = hematoxylin and eosin; HW = heart weight; LVEF = left ventricular ejection fraction; TGF = transforming growth factor; TUNEL = terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling; other abbreviations as in Figure 1 .

    Article Snippet: After rehydration in citrate buffer solution and a 40-minute antigen recovery process, mouse heart slices were permeabilized with 0.2% Triton X-100 in PBS for 15 minutes, sealed with 5% bovine serum albumin for 1 hour, and stained overnight with Trim55 (1:50, Thermo Fisher Scientific) antibody.

    Techniques: Knock-Out, Staining, Western Blot, Expressing, TUNEL Assay, End Labeling

    Trim55 Overexpression Promoted Cardiomyocyte Apoptosis Induced by Hypoxia (A, B) Quantification and representative images of Western blots showing the expression of apoptosis-related proteins after Trim55 overexpression (n = 3). (C, D) Effects of Trim55 overexpression and CoCl treatment on the expression of apoptosis-related proteins by Western blot (n = 3). (E, F) Effects of Trim55 overexpression and CoCl treatment on cardiomyocyte apoptosis by flow cytometry analysis (n = 4). (G, H) Effects of Trim55 overexpression and CoCl treatment on cardiomyocyte apoptosis by TUNEL staining (n = 3). CoCl : 400 μmol/L, 24 hours. All data in B, D, F, and H are expressed as mean ± SEM. Data in B were analyzed using an unpaired Student’s t -test. Data in D, F, and H were analyzed using 2-way analysis of variance followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon; † P < 0.05 vs adTrim55; ‡ P < 0.05 vs adcon + CoCl . adcon = adenovirus control; adTrim55 = Trim55-overexpressing adenovirus; DAPI = 4′,6-diamidino-2-phenylindole; ns = not significant; other abbreviations as in <xref ref-type=Figures 1 and . " width="100%" height="100%">

    Journal: JACC: Basic to Translational Science

    Article Title: TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway

    doi: 10.1016/j.jacbts.2024.05.006

    Figure Lengend Snippet: Trim55 Overexpression Promoted Cardiomyocyte Apoptosis Induced by Hypoxia (A, B) Quantification and representative images of Western blots showing the expression of apoptosis-related proteins after Trim55 overexpression (n = 3). (C, D) Effects of Trim55 overexpression and CoCl treatment on the expression of apoptosis-related proteins by Western blot (n = 3). (E, F) Effects of Trim55 overexpression and CoCl treatment on cardiomyocyte apoptosis by flow cytometry analysis (n = 4). (G, H) Effects of Trim55 overexpression and CoCl treatment on cardiomyocyte apoptosis by TUNEL staining (n = 3). CoCl : 400 μmol/L, 24 hours. All data in B, D, F, and H are expressed as mean ± SEM. Data in B were analyzed using an unpaired Student’s t -test. Data in D, F, and H were analyzed using 2-way analysis of variance followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon; † P < 0.05 vs adTrim55; ‡ P < 0.05 vs adcon + CoCl . adcon = adenovirus control; adTrim55 = Trim55-overexpressing adenovirus; DAPI = 4′,6-diamidino-2-phenylindole; ns = not significant; other abbreviations as in Figures 1 and .

    Article Snippet: After rehydration in citrate buffer solution and a 40-minute antigen recovery process, mouse heart slices were permeabilized with 0.2% Triton X-100 in PBS for 15 minutes, sealed with 5% bovine serum albumin for 1 hour, and stained overnight with Trim55 (1:50, Thermo Fisher Scientific) antibody.

    Techniques: Over Expression, Western Blot, Expressing, Flow Cytometry, TUNEL Assay, Staining, Control

    Trim55 Knockdown Alleviated Cardiomyocyte Apoptosis Induced by Hypoxia (A, B) Quantification and representative images of Western blot analyses showing the expression of apoptosis-related proteins after Trim55 knockdown (n = 3). (C, D) Effects of Trim55 knockdown and CoCl 2 treatment on the expression of apoptosis-related proteins by Western blot (n = 3). (E, F) Effects of Trim55 knockout and CoCl 2 treatment on cardiomyocyte apoptosis by flow cytometry analysis (n = 4). (G, H) Effects of Trim55 knockdown and CoCl 2 treatment on cardiomyocyte apoptosis by TUNEL staining (n = 3). All data in B, D, F, and H are expressed as mean ± SEM. Data in B were analyzed using an unpaired Student’s t -test. Data in D, F, and H were analyzed using 2-way analysis of variance, followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs si-nc; ‡ P < 0.05 vs si-Trim55; † P < 0.05 vs si-nc + CoCl 2 . si-nc = siRNA-normal control; si-Trim55 = Trim55-interfering RNA; other abbreviations as in <xref ref-type=Figure 1 , Figure 2 , Figure 3 . " width="100%" height="100%">

    Journal: JACC: Basic to Translational Science

    Article Title: TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway

    doi: 10.1016/j.jacbts.2024.05.006

    Figure Lengend Snippet: Trim55 Knockdown Alleviated Cardiomyocyte Apoptosis Induced by Hypoxia (A, B) Quantification and representative images of Western blot analyses showing the expression of apoptosis-related proteins after Trim55 knockdown (n = 3). (C, D) Effects of Trim55 knockdown and CoCl 2 treatment on the expression of apoptosis-related proteins by Western blot (n = 3). (E, F) Effects of Trim55 knockout and CoCl 2 treatment on cardiomyocyte apoptosis by flow cytometry analysis (n = 4). (G, H) Effects of Trim55 knockdown and CoCl 2 treatment on cardiomyocyte apoptosis by TUNEL staining (n = 3). All data in B, D, F, and H are expressed as mean ± SEM. Data in B were analyzed using an unpaired Student’s t -test. Data in D, F, and H were analyzed using 2-way analysis of variance, followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs si-nc; ‡ P < 0.05 vs si-Trim55; † P < 0.05 vs si-nc + CoCl 2 . si-nc = siRNA-normal control; si-Trim55 = Trim55-interfering RNA; other abbreviations as in Figure 1 , Figure 2 , Figure 3 .

    Article Snippet: After rehydration in citrate buffer solution and a 40-minute antigen recovery process, mouse heart slices were permeabilized with 0.2% Triton X-100 in PBS for 15 minutes, sealed with 5% bovine serum albumin for 1 hour, and stained overnight with Trim55 (1:50, Thermo Fisher Scientific) antibody.

    Techniques: Knockdown, Western Blot, Expressing, Knock-Out, Flow Cytometry, TUNEL Assay, Staining, Control

    Trim55 Promoted Oxidative Stress by Inhibiting the Nrf2/HO-1 Pathway in Cardiomyocytes (A) Quantification and representative images of Western blot analyses showing the expression of antioxidant proteins (P62, Nrf2, HO-1) after overexpression of Trim55 in cardiomyocytes (n = 3). (B) Quantification and representative images of Western blot analyses showing the expression of antioxidant proteins (P62, Nrf2, HO-1) after Trim55 knockdown (n = 3). (C) Effects of Trim55 overexpression on the intracellular ROS levels by flow cytometry (n = 5). (D) Effects of Trim55 silencing on the intracellular ROS levels by flow cytometry (n = 5). (E) Quantification and representative images of CellROX staining after Trim55 overexpression (n = 3). (F) Quantification and representative images of CellROX staining after Trim55 knockdown (n = 3). All data in A to F are expressed as mean ±SEM. Data in A to F were analyzed by Student’s t -test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon or si-nc. APC = allophycocyanin; HO-1 = heme oxygenase 1; ISO = isotype control; Nrf2 = nuclear factor, erythroid derived 2; ROS = reactive oxygen species; other abbreviations as in <xref ref-type=Figure 1 , Figure 2 , Figure 3 , Figure 4 . " width="100%" height="100%">

    Journal: JACC: Basic to Translational Science

    Article Title: TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway

    doi: 10.1016/j.jacbts.2024.05.006

    Figure Lengend Snippet: Trim55 Promoted Oxidative Stress by Inhibiting the Nrf2/HO-1 Pathway in Cardiomyocytes (A) Quantification and representative images of Western blot analyses showing the expression of antioxidant proteins (P62, Nrf2, HO-1) after overexpression of Trim55 in cardiomyocytes (n = 3). (B) Quantification and representative images of Western blot analyses showing the expression of antioxidant proteins (P62, Nrf2, HO-1) after Trim55 knockdown (n = 3). (C) Effects of Trim55 overexpression on the intracellular ROS levels by flow cytometry (n = 5). (D) Effects of Trim55 silencing on the intracellular ROS levels by flow cytometry (n = 5). (E) Quantification and representative images of CellROX staining after Trim55 overexpression (n = 3). (F) Quantification and representative images of CellROX staining after Trim55 knockdown (n = 3). All data in A to F are expressed as mean ±SEM. Data in A to F were analyzed by Student’s t -test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon or si-nc. APC = allophycocyanin; HO-1 = heme oxygenase 1; ISO = isotype control; Nrf2 = nuclear factor, erythroid derived 2; ROS = reactive oxygen species; other abbreviations as in Figure 1 , Figure 2 , Figure 3 , Figure 4 .

    Article Snippet: After rehydration in citrate buffer solution and a 40-minute antigen recovery process, mouse heart slices were permeabilized with 0.2% Triton X-100 in PBS for 15 minutes, sealed with 5% bovine serum albumin for 1 hour, and stained overnight with Trim55 (1:50, Thermo Fisher Scientific) antibody.

    Techniques: Western Blot, Expressing, Over Expression, Knockdown, Flow Cytometry, Staining, Control, Derivative Assay

    Trim55 Promoted Cardiomyocyte Apoptosis Through Inhibiting the Nrf2/HO-1 Signaling Pathway (A) Effects of Trim55 overexpression and HO-1 overexpression on the expression of Trim55, HO-1, cleaved caspase-3, and cleaved caspase-8 by Western blot (n = 3). (B) Effects of Trim55 overexpression and HO-1 overexpression on cardiomyocyte apoptosis by flow cytometry (n = 4). (C) Effects of Trim55 overexpression and HO-1 overexpression on cardiomyocyte apoptosis by TUNEL staining (n = 3). (D) Effects of Trim55 knockdown and HO-1 knockdown on the expressions of cleaved caspase-3 and cleaved caspase-8 by Western blot (n = 3). (E) Effects of Trim55 knockdown and HO-1 knockdown on cardiomyocyte apoptosis by flow cytometry (n = 4). (F) Effects of Trim55 knockdown and HO-1 knockdown on cardiomyocyte apoptosis by TUNEL staining (n = 3). All data in A to F are expressed as mean ± SEM. Data in A to F were analyzed by 2-way analysis of variance followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon or si-nc; † P < 0.05 vs adTrim55 or si-nc + si HO-1; ‡ P < 0.05 vs adcon + pcDNA3.1 HO-1 or si-Trim55. Abbreviations as in <xref ref-type=Figure 1 , Figure 2 , Figure 3 , Figure 4 , Figure 5 . " width="100%" height="100%">

    Journal: JACC: Basic to Translational Science

    Article Title: TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway

    doi: 10.1016/j.jacbts.2024.05.006

    Figure Lengend Snippet: Trim55 Promoted Cardiomyocyte Apoptosis Through Inhibiting the Nrf2/HO-1 Signaling Pathway (A) Effects of Trim55 overexpression and HO-1 overexpression on the expression of Trim55, HO-1, cleaved caspase-3, and cleaved caspase-8 by Western blot (n = 3). (B) Effects of Trim55 overexpression and HO-1 overexpression on cardiomyocyte apoptosis by flow cytometry (n = 4). (C) Effects of Trim55 overexpression and HO-1 overexpression on cardiomyocyte apoptosis by TUNEL staining (n = 3). (D) Effects of Trim55 knockdown and HO-1 knockdown on the expressions of cleaved caspase-3 and cleaved caspase-8 by Western blot (n = 3). (E) Effects of Trim55 knockdown and HO-1 knockdown on cardiomyocyte apoptosis by flow cytometry (n = 4). (F) Effects of Trim55 knockdown and HO-1 knockdown on cardiomyocyte apoptosis by TUNEL staining (n = 3). All data in A to F are expressed as mean ± SEM. Data in A to F were analyzed by 2-way analysis of variance followed by the Bonferroni post hoc test. ∗ P < 0.05, ∗∗ P < 0.01 vs adcon or si-nc; † P < 0.05 vs adTrim55 or si-nc + si HO-1; ‡ P < 0.05 vs adcon + pcDNA3.1 HO-1 or si-Trim55. Abbreviations as in Figure 1 , Figure 2 , Figure 3 , Figure 4 , Figure 5 .

    Article Snippet: After rehydration in citrate buffer solution and a 40-minute antigen recovery process, mouse heart slices were permeabilized with 0.2% Triton X-100 in PBS for 15 minutes, sealed with 5% bovine serum albumin for 1 hour, and stained overnight with Trim55 (1:50, Thermo Fisher Scientific) antibody.

    Techniques: Over Expression, Expressing, Western Blot, Flow Cytometry, TUNEL Assay, Staining, Knockdown

    Foxo3 Was a Direct Upstream Transcription Factor of Trim55 (A, B) Quantification and representative images of Western blots showing the expression of Foxo3, Gata3, Hoxa5, and Stat3 after CoCl 2 hypoxia in NRCMs (n = 3). ∗ P < 0.05 vs CON. (C, D) Foxo3 expression in the myocardium post-MI. (n = 3). ∗ P < 0.05, ∗∗ P < 0.01 vs sham (E, F) Quantification and representative images of Western blot analyses showing the expression of Trim55 after Foxo3 overexpression in NRCMs (n = 3). ∗∗ P < 0.01 vs CON. (G) Quantification of Trim55 mRNA levels in NRCMs after Foxo3 overexpression (n = 3). ∗∗ P < 0.01 vs CON. (H, I) Quantification and representative images of Western blot analyses showing the expression of Trim55 after knockdown in NRCMs (n = 3). † P < 0.05 vs si-nc. (J) Quantification of Trim55 mRNA levels in NRCMs after Foxo3 knockdown (n = 3). † P < 0.05 vs si-nc. (K) Possible binding sites of Foxo3 and Trim55 were predicted using the JASPAR website. (L) Relative luciferase activity in HEK293T cells with cotransfection with Foxo3-overexpressing plasmid and with WT-Trim55 plasmid or Mut-Trim55 plasmid. ∗∗ P < 0.01 vs NC Foxo3 + WT-Trim55; ‡ P < 0.05 vs NC Foxo3 + Mut-Trim55 (n = 12). (M) The effect of Trim55 on cardiomyocyte apoptosis after MI (by Figdraw). All data in B, D, F, G, H, and J are expressed as mean ± SEM. Data in B, D, F, G, and H were analyzed using Student’s t -test. Data in J were analyzed using 2-way analysis of variance, followed by the Bonferroni post hoc test. Foxo3 = forkhead box transcription factor 3; Mut = mutated; NC = normal control; WT = wild type; other abbreviations as in <xref ref-type=Figure 1 , Figure 2 , Figure 3 , Figure 4 , Figure 5 . " width="100%" height="100%">

    Journal: JACC: Basic to Translational Science

    Article Title: TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway

    doi: 10.1016/j.jacbts.2024.05.006

    Figure Lengend Snippet: Foxo3 Was a Direct Upstream Transcription Factor of Trim55 (A, B) Quantification and representative images of Western blots showing the expression of Foxo3, Gata3, Hoxa5, and Stat3 after CoCl 2 hypoxia in NRCMs (n = 3). ∗ P < 0.05 vs CON. (C, D) Foxo3 expression in the myocardium post-MI. (n = 3). ∗ P < 0.05, ∗∗ P < 0.01 vs sham (E, F) Quantification and representative images of Western blot analyses showing the expression of Trim55 after Foxo3 overexpression in NRCMs (n = 3). ∗∗ P < 0.01 vs CON. (G) Quantification of Trim55 mRNA levels in NRCMs after Foxo3 overexpression (n = 3). ∗∗ P < 0.01 vs CON. (H, I) Quantification and representative images of Western blot analyses showing the expression of Trim55 after knockdown in NRCMs (n = 3). † P < 0.05 vs si-nc. (J) Quantification of Trim55 mRNA levels in NRCMs after Foxo3 knockdown (n = 3). † P < 0.05 vs si-nc. (K) Possible binding sites of Foxo3 and Trim55 were predicted using the JASPAR website. (L) Relative luciferase activity in HEK293T cells with cotransfection with Foxo3-overexpressing plasmid and with WT-Trim55 plasmid or Mut-Trim55 plasmid. ∗∗ P < 0.01 vs NC Foxo3 + WT-Trim55; ‡ P < 0.05 vs NC Foxo3 + Mut-Trim55 (n = 12). (M) The effect of Trim55 on cardiomyocyte apoptosis after MI (by Figdraw). All data in B, D, F, G, H, and J are expressed as mean ± SEM. Data in B, D, F, G, and H were analyzed using Student’s t -test. Data in J were analyzed using 2-way analysis of variance, followed by the Bonferroni post hoc test. Foxo3 = forkhead box transcription factor 3; Mut = mutated; NC = normal control; WT = wild type; other abbreviations as in Figure 1 , Figure 2 , Figure 3 , Figure 4 , Figure 5 .

    Article Snippet: After rehydration in citrate buffer solution and a 40-minute antigen recovery process, mouse heart slices were permeabilized with 0.2% Triton X-100 in PBS for 15 minutes, sealed with 5% bovine serum albumin for 1 hour, and stained overnight with Trim55 (1:50, Thermo Fisher Scientific) antibody.

    Techniques: Western Blot, Expressing, Over Expression, Knockdown, Binding Assay, Luciferase, Activity Assay, Cotransfection, Plasmid Preparation, Control

    Representative images of immunohistochemical staining for TRIM55 in human gastric cancer tissue and its prognostic significance. A: Low expression of TRIM55 in gastric normal mucosa tissue; B: TRIM55 expression in well-differentiated adenocarcinoma; C: TRIM55 expression in poorly differentiated adenocarcinoma; D: Overexpression of TRIM55 in signet-ring cell carcinoma. Original magnification, 400 ×; E: TRIM55 protein levels in five tumor samples and their matched normal tissues; F: Overall survival curves for 91 gastric cancer (GC) patients according to TRIM55 protein expression ( P = 0.026); G: Overall survival curves of TCGA GC patients with different TRIM55 expression. c P < 0.001. HR: Hazard ratio; GC: Gastric cancer.

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: E3 ubiquitin ligase TRIM55 promotes metastasis of gastric cancer cells by mediating epithelial-mesenchymal transition

    doi: 10.4251/wjgo.v14.i11.2183

    Figure Lengend Snippet: Representative images of immunohistochemical staining for TRIM55 in human gastric cancer tissue and its prognostic significance. A: Low expression of TRIM55 in gastric normal mucosa tissue; B: TRIM55 expression in well-differentiated adenocarcinoma; C: TRIM55 expression in poorly differentiated adenocarcinoma; D: Overexpression of TRIM55 in signet-ring cell carcinoma. Original magnification, 400 ×; E: TRIM55 protein levels in five tumor samples and their matched normal tissues; F: Overall survival curves for 91 gastric cancer (GC) patients according to TRIM55 protein expression ( P = 0.026); G: Overall survival curves of TCGA GC patients with different TRIM55 expression. c P < 0.001. HR: Hazard ratio; GC: Gastric cancer.

    Article Snippet: TRIM55 primary antibody (Novus, United States) was added and incubated overnight at 4 °C.

    Techniques: Immunohistochemical staining, Staining, Expressing, Over Expression

    Association between  TRIM55  expression and clinicopathological characteristics

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: E3 ubiquitin ligase TRIM55 promotes metastasis of gastric cancer cells by mediating epithelial-mesenchymal transition

    doi: 10.4251/wjgo.v14.i11.2183

    Figure Lengend Snippet: Association between TRIM55 expression and clinicopathological characteristics

    Article Snippet: TRIM55 primary antibody (Novus, United States) was added and incubated overnight at 4 °C.

    Techniques: Expressing

    Univariate and multivariate Cox regression models for estimating the overall survival

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: E3 ubiquitin ligase TRIM55 promotes metastasis of gastric cancer cells by mediating epithelial-mesenchymal transition

    doi: 10.4251/wjgo.v14.i11.2183

    Figure Lengend Snippet: Univariate and multivariate Cox regression models for estimating the overall survival

    Article Snippet: TRIM55 primary antibody (Novus, United States) was added and incubated overnight at 4 °C.

    Techniques:

    TRIM55 expression in gastric cancer cells. A: The expression of TRIM protein was detected in gastric cancer (GC) cells by western blot. The histogram shows the expression of TRIM55 in GC cells was stronger than that in gastric mucosa cell line; B: The interference efficiency of TRIM55 small interfering RNA (siRNA) in SGC7901 cells was detected by Western blot; C: Quantitative real-time-polymerase chain reaction assay was performed to determine TRIM55 expression after transfection with siRNA; D: The up-regulation of TRIM55 expression in HGC27 cells was detected by Western blot; E: TRIM55 mRNA expression level in HGC27 after transfection with the TRIM55 plasmid. b P < 0.01; c P < 0.001.

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: E3 ubiquitin ligase TRIM55 promotes metastasis of gastric cancer cells by mediating epithelial-mesenchymal transition

    doi: 10.4251/wjgo.v14.i11.2183

    Figure Lengend Snippet: TRIM55 expression in gastric cancer cells. A: The expression of TRIM protein was detected in gastric cancer (GC) cells by western blot. The histogram shows the expression of TRIM55 in GC cells was stronger than that in gastric mucosa cell line; B: The interference efficiency of TRIM55 small interfering RNA (siRNA) in SGC7901 cells was detected by Western blot; C: Quantitative real-time-polymerase chain reaction assay was performed to determine TRIM55 expression after transfection with siRNA; D: The up-regulation of TRIM55 expression in HGC27 cells was detected by Western blot; E: TRIM55 mRNA expression level in HGC27 after transfection with the TRIM55 plasmid. b P < 0.01; c P < 0.001.

    Article Snippet: TRIM55 primary antibody (Novus, United States) was added and incubated overnight at 4 °C.

    Techniques: Expressing, Western Blot, Small Interfering RNA, Real-time Polymerase Chain Reaction, Transfection, Plasmid Preparation

    TRIM55 regulates gastric cancer cell proliferation. A and B: Cell viability detected by cell counting kit-8 assay in SGC7901 cells after knockdown of TRIM55 and in HGC27 cells after overexpression of TRIM55 ; C and D: Colony formation analysis of TRIM55 knockdown-treated SGC7901 cells and TRIM55 overexpression-treated HGC27 cells. c P < 0.001.

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: E3 ubiquitin ligase TRIM55 promotes metastasis of gastric cancer cells by mediating epithelial-mesenchymal transition

    doi: 10.4251/wjgo.v14.i11.2183

    Figure Lengend Snippet: TRIM55 regulates gastric cancer cell proliferation. A and B: Cell viability detected by cell counting kit-8 assay in SGC7901 cells after knockdown of TRIM55 and in HGC27 cells after overexpression of TRIM55 ; C and D: Colony formation analysis of TRIM55 knockdown-treated SGC7901 cells and TRIM55 overexpression-treated HGC27 cells. c P < 0.001.

    Article Snippet: TRIM55 primary antibody (Novus, United States) was added and incubated overnight at 4 °C.

    Techniques: Cell Counting, Knockdown, Over Expression

    TRIM55 promotes metastasis of gastric cancer cells. A: Migration and invasion analysis of TRIM55 knockdown-treated SGC7901 cells; B: Migration and invasion analysis of TRIM55 overexpression treated-HGC27 cells. c P < 0.001.

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: E3 ubiquitin ligase TRIM55 promotes metastasis of gastric cancer cells by mediating epithelial-mesenchymal transition

    doi: 10.4251/wjgo.v14.i11.2183

    Figure Lengend Snippet: TRIM55 promotes metastasis of gastric cancer cells. A: Migration and invasion analysis of TRIM55 knockdown-treated SGC7901 cells; B: Migration and invasion analysis of TRIM55 overexpression treated-HGC27 cells. c P < 0.001.

    Article Snippet: TRIM55 primary antibody (Novus, United States) was added and incubated overnight at 4 °C.

    Techniques: Migration, Knockdown, Over Expression

    Wound healing assays were performed in gastric cancer cells. A: Migration rates of SGC7901 cells at 24 h were lower than that in control groups after knockdown of TRIM55 ; B: Migration rates of HGC27 cells at 24 h were higher than that in control groups after overexpression of TRIM55 . c P < 0.001.

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: E3 ubiquitin ligase TRIM55 promotes metastasis of gastric cancer cells by mediating epithelial-mesenchymal transition

    doi: 10.4251/wjgo.v14.i11.2183

    Figure Lengend Snippet: Wound healing assays were performed in gastric cancer cells. A: Migration rates of SGC7901 cells at 24 h were lower than that in control groups after knockdown of TRIM55 ; B: Migration rates of HGC27 cells at 24 h were higher than that in control groups after overexpression of TRIM55 . c P < 0.001.

    Article Snippet: TRIM55 primary antibody (Novus, United States) was added and incubated overnight at 4 °C.

    Techniques: Migration, Control, Knockdown, Over Expression

    Western blot results of epithelial-mesenchymal transition pathway-related proteins in gastric cancer cells. A and B: Western blot analysis of E-cadherin, N-cadherin, Vimentin, ZEB1, and Snail after TRIM55 knockdown and overexpression in SGC7901 and HGC27 cells; C: Histogram of the expression of E-cadherin, N-cadherin, Vimentin, Snail, and ZEB1 proteins related to metastasis after knockdown or overexpression of TRIM55 . c P < 0.001.

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: E3 ubiquitin ligase TRIM55 promotes metastasis of gastric cancer cells by mediating epithelial-mesenchymal transition

    doi: 10.4251/wjgo.v14.i11.2183

    Figure Lengend Snippet: Western blot results of epithelial-mesenchymal transition pathway-related proteins in gastric cancer cells. A and B: Western blot analysis of E-cadherin, N-cadherin, Vimentin, ZEB1, and Snail after TRIM55 knockdown and overexpression in SGC7901 and HGC27 cells; C: Histogram of the expression of E-cadherin, N-cadherin, Vimentin, Snail, and ZEB1 proteins related to metastasis after knockdown or overexpression of TRIM55 . c P < 0.001.

    Article Snippet: TRIM55 primary antibody (Novus, United States) was added and incubated overnight at 4 °C.

    Techniques: Western Blot, Knockdown, Over Expression, Expressing

    Figure 1. TRIM55 is downregulated in HCC tissues and is associated with prognosis of HCC patients. (A) IHC detected expression of TRIM55 in HCC tissues and neighboring tissues. Representative photos at 200× and 400×. The level of TRIM55 expression between HCC tissues and neighbor tissues was analyzed and shown as a pie chart. (B, C) the relationship between overall survival and TRIM55 expression was analyzed by Kaplan-Meier analysis, and the follow-up data were collected by ourselves (B) or TCGA database (C).

    Journal: Medical Science Monitor

    Article Title: Overexpression of Tripartite Motif Conaining 55 (TRIM55) Inhibits Migration and Invasion of Hepatocellular Carcinoma (HCC) Cells via Epithelial-Mesenchymal Transition and Matrix Metalloproteinase-2 (MMP2)

    doi: 10.12659/msm.910984

    Figure Lengend Snippet: Figure 1. TRIM55 is downregulated in HCC tissues and is associated with prognosis of HCC patients. (A) IHC detected expression of TRIM55 in HCC tissues and neighboring tissues. Representative photos at 200× and 400×. The level of TRIM55 expression between HCC tissues and neighbor tissues was analyzed and shown as a pie chart. (B, C) the relationship between overall survival and TRIM55 expression was analyzed by Kaplan-Meier analysis, and the follow-up data were collected by ourselves (B) or TCGA database (C).

    Article Snippet: The primary antibodies were as follows: TRIM55 (Novus, NBP2-33691, dilution 1/1000), E-cadherin and Vimentin (Cell Signaling Technology, (EMT) Antibody Sampler Kit #9782, dilution 1/1000), and MMP2 (Proteintech, 10373-2-AP, dilution 1/1000), and the internal control was GAPDH (Abcam Biotechnology, Cambridge, UK, dilution 1/1000).

    Techniques: Expressing

    Figure 2. TRIM55 overexpression in HCC cell lines was constructed. (A) Western blot was used to verify transfection efficiency at the protein level. GAPDH was used as internal control. (B) RT-PCR was used to verify transfection efficiency at the mRNA level, *** p<0.0001.

    Journal: Medical Science Monitor

    Article Title: Overexpression of Tripartite Motif Conaining 55 (TRIM55) Inhibits Migration and Invasion of Hepatocellular Carcinoma (HCC) Cells via Epithelial-Mesenchymal Transition and Matrix Metalloproteinase-2 (MMP2)

    doi: 10.12659/msm.910984

    Figure Lengend Snippet: Figure 2. TRIM55 overexpression in HCC cell lines was constructed. (A) Western blot was used to verify transfection efficiency at the protein level. GAPDH was used as internal control. (B) RT-PCR was used to verify transfection efficiency at the mRNA level, *** p<0.0001.

    Article Snippet: The primary antibodies were as follows: TRIM55 (Novus, NBP2-33691, dilution 1/1000), E-cadherin and Vimentin (Cell Signaling Technology, (EMT) Antibody Sampler Kit #9782, dilution 1/1000), and MMP2 (Proteintech, 10373-2-AP, dilution 1/1000), and the internal control was GAPDH (Abcam Biotechnology, Cambridge, UK, dilution 1/1000).

    Techniques: Over Expression, Construct, Western Blot, Transfection, Control, Reverse Transcription Polymerase Chain Reaction

    Figure 3. Overexpression of TRIM55 inhibits migration and invasion of HCC cells. (A, B) Cell migration and invasion ability were detected by Transwell assay in HCC cells with TRIM55 overexpression and negative control. All experiments were repeated 3 times. *** p<0.0001

    Journal: Medical Science Monitor

    Article Title: Overexpression of Tripartite Motif Conaining 55 (TRIM55) Inhibits Migration and Invasion of Hepatocellular Carcinoma (HCC) Cells via Epithelial-Mesenchymal Transition and Matrix Metalloproteinase-2 (MMP2)

    doi: 10.12659/msm.910984

    Figure Lengend Snippet: Figure 3. Overexpression of TRIM55 inhibits migration and invasion of HCC cells. (A, B) Cell migration and invasion ability were detected by Transwell assay in HCC cells with TRIM55 overexpression and negative control. All experiments were repeated 3 times. *** p<0.0001

    Article Snippet: The primary antibodies were as follows: TRIM55 (Novus, NBP2-33691, dilution 1/1000), E-cadherin and Vimentin (Cell Signaling Technology, (EMT) Antibody Sampler Kit #9782, dilution 1/1000), and MMP2 (Proteintech, 10373-2-AP, dilution 1/1000), and the internal control was GAPDH (Abcam Biotechnology, Cambridge, UK, dilution 1/1000).

    Techniques: Over Expression, Migration, Transwell Assay, Negative Control

    Figure 4. Overexpression of TRIM55 inhibits migration and invasion of HCC cells through EMT and MMP2. (A) IF was used to detect expression of E-cadherin and Vimentin in HCC cells with TRIM55 overexpression and negative control. (B) Western blot was used to detect expression of E-cadherin, Vimentin, and MMP2 in HCC cells with TRIM55 overexpression and negative control. GAPDH was used as internal control.

    Journal: Medical Science Monitor

    Article Title: Overexpression of Tripartite Motif Conaining 55 (TRIM55) Inhibits Migration and Invasion of Hepatocellular Carcinoma (HCC) Cells via Epithelial-Mesenchymal Transition and Matrix Metalloproteinase-2 (MMP2)

    doi: 10.12659/msm.910984

    Figure Lengend Snippet: Figure 4. Overexpression of TRIM55 inhibits migration and invasion of HCC cells through EMT and MMP2. (A) IF was used to detect expression of E-cadherin and Vimentin in HCC cells with TRIM55 overexpression and negative control. (B) Western blot was used to detect expression of E-cadherin, Vimentin, and MMP2 in HCC cells with TRIM55 overexpression and negative control. GAPDH was used as internal control.

    Article Snippet: The primary antibodies were as follows: TRIM55 (Novus, NBP2-33691, dilution 1/1000), E-cadherin and Vimentin (Cell Signaling Technology, (EMT) Antibody Sampler Kit #9782, dilution 1/1000), and MMP2 (Proteintech, 10373-2-AP, dilution 1/1000), and the internal control was GAPDH (Abcam Biotechnology, Cambridge, UK, dilution 1/1000).

    Techniques: Over Expression, Migration, Expressing, Negative Control, Western Blot, Control

    Figure 1. TRIM55 is downregulated in HCC tissues and is associated with prognosis of HCC patients. (A) IHC detected expression of TRIM55 in HCC tissues and neighboring tissues. Representative photos at 200× and 400×. The level of TRIM55 expression between HCC tissues and neighbor tissues was analyzed and shown as a pie chart. (B, C) the relationship between overall survival and TRIM55 expression was analyzed by Kaplan-Meier analysis, and the follow-up data were collected by ourselves (B) or TCGA database (C).

    Journal: Medical Science Monitor

    Article Title: Overexpression of Tripartite Motif Conaining 55 (TRIM55) Inhibits Migration and Invasion of Hepatocellular Carcinoma (HCC) Cells via Epithelial-Mesenchymal Transition and Matrix Metalloproteinase-2 (MMP2)

    doi: 10.12659/msm.910984

    Figure Lengend Snippet: Figure 1. TRIM55 is downregulated in HCC tissues and is associated with prognosis of HCC patients. (A) IHC detected expression of TRIM55 in HCC tissues and neighboring tissues. Representative photos at 200× and 400×. The level of TRIM55 expression between HCC tissues and neighbor tissues was analyzed and shown as a pie chart. (B, C) the relationship between overall survival and TRIM55 expression was analyzed by Kaplan-Meier analysis, and the follow-up data were collected by ourselves (B) or TCGA database (C).

    Article Snippet: After exposure to 5% BSA for 30 min, all tissues were incubated with rabbit antibody to human TRIM55 antibody (Novus, NBP2-33691, dilution 1/200) overnight at 4°C.

    Techniques: Expressing

    Figure 2. TRIM55 overexpression in HCC cell lines was constructed. (A) Western blot was used to verify transfection efficiency at the protein level. GAPDH was used as internal control. (B) RT-PCR was used to verify transfection efficiency at the mRNA level, *** p<0.0001.

    Journal: Medical Science Monitor

    Article Title: Overexpression of Tripartite Motif Conaining 55 (TRIM55) Inhibits Migration and Invasion of Hepatocellular Carcinoma (HCC) Cells via Epithelial-Mesenchymal Transition and Matrix Metalloproteinase-2 (MMP2)

    doi: 10.12659/msm.910984

    Figure Lengend Snippet: Figure 2. TRIM55 overexpression in HCC cell lines was constructed. (A) Western blot was used to verify transfection efficiency at the protein level. GAPDH was used as internal control. (B) RT-PCR was used to verify transfection efficiency at the mRNA level, *** p<0.0001.

    Article Snippet: After exposure to 5% BSA for 30 min, all tissues were incubated with rabbit antibody to human TRIM55 antibody (Novus, NBP2-33691, dilution 1/200) overnight at 4°C.

    Techniques: Over Expression, Construct, Western Blot, Transfection, Control, Reverse Transcription Polymerase Chain Reaction

    Figure 3. Overexpression of TRIM55 inhibits migration and invasion of HCC cells. (A, B) Cell migration and invasion ability were detected by Transwell assay in HCC cells with TRIM55 overexpression and negative control. All experiments were repeated 3 times. *** p<0.0001

    Journal: Medical Science Monitor

    Article Title: Overexpression of Tripartite Motif Conaining 55 (TRIM55) Inhibits Migration and Invasion of Hepatocellular Carcinoma (HCC) Cells via Epithelial-Mesenchymal Transition and Matrix Metalloproteinase-2 (MMP2)

    doi: 10.12659/msm.910984

    Figure Lengend Snippet: Figure 3. Overexpression of TRIM55 inhibits migration and invasion of HCC cells. (A, B) Cell migration and invasion ability were detected by Transwell assay in HCC cells with TRIM55 overexpression and negative control. All experiments were repeated 3 times. *** p<0.0001

    Article Snippet: After exposure to 5% BSA for 30 min, all tissues were incubated with rabbit antibody to human TRIM55 antibody (Novus, NBP2-33691, dilution 1/200) overnight at 4°C.

    Techniques: Over Expression, Migration, Transwell Assay, Negative Control

    Figure 4. Overexpression of TRIM55 inhibits migration and invasion of HCC cells through EMT and MMP2. (A) IF was used to detect expression of E-cadherin and Vimentin in HCC cells with TRIM55 overexpression and negative control. (B) Western blot was used to detect expression of E-cadherin, Vimentin, and MMP2 in HCC cells with TRIM55 overexpression and negative control. GAPDH was used as internal control.

    Journal: Medical Science Monitor

    Article Title: Overexpression of Tripartite Motif Conaining 55 (TRIM55) Inhibits Migration and Invasion of Hepatocellular Carcinoma (HCC) Cells via Epithelial-Mesenchymal Transition and Matrix Metalloproteinase-2 (MMP2)

    doi: 10.12659/msm.910984

    Figure Lengend Snippet: Figure 4. Overexpression of TRIM55 inhibits migration and invasion of HCC cells through EMT and MMP2. (A) IF was used to detect expression of E-cadherin and Vimentin in HCC cells with TRIM55 overexpression and negative control. (B) Western blot was used to detect expression of E-cadherin, Vimentin, and MMP2 in HCC cells with TRIM55 overexpression and negative control. GAPDH was used as internal control.

    Article Snippet: After exposure to 5% BSA for 30 min, all tissues were incubated with rabbit antibody to human TRIM55 antibody (Novus, NBP2-33691, dilution 1/200) overnight at 4°C.

    Techniques: Over Expression, Migration, Expressing, Negative Control, Western Blot, Control

    Fig. 1 MuRF1 and MuRF2 are highly induced during skeletal muscle regeneration. (a) MuRF1, MuRF2 and Mafbx/Atrogin‐1 immunoblots 3 and 10 days after TA CTX injury. Sarcomeric actin is a loading control. (b‐g) Immunolocalization of MuRF1 and (j‐o) MuRF2, 3 and 10 days after CTX injury in TA muscle. In h‐i and p‐q, primary antibodies were not used in the assay. Immunodetection of laminin (green) was used to outline muscle fibers. (h‐i and p‐q) No primary antibodies were added to the assay. Images were obtained with a fluorescence microscope and a 40x air medium objective. Bar, 50µm

    Journal: JCSM Rapid Communications

    Article Title: MuRF1 and MuRF2 are key players in skeletal muscle regeneration involving myogenic deficit and deregulation of the chromatin-remodeling complex

    doi: 10.1002/j.2617-1619.2019.tb00010.x

    Figure Lengend Snippet: Fig. 1 MuRF1 and MuRF2 are highly induced during skeletal muscle regeneration. (a) MuRF1, MuRF2 and Mafbx/Atrogin‐1 immunoblots 3 and 10 days after TA CTX injury. Sarcomeric actin is a loading control. (b‐g) Immunolocalization of MuRF1 and (j‐o) MuRF2, 3 and 10 days after CTX injury in TA muscle. In h‐i and p‐q, primary antibodies were not used in the assay. Immunodetection of laminin (green) was used to outline muscle fibers. (h‐i and p‐q) No primary antibodies were added to the assay. Images were obtained with a fluorescence microscope and a 40x air medium objective. Bar, 50µm

    Article Snippet: The primary antibodies used for immunofluorescence were: (1) MuRF1 and (2) MuRF2 [27, 32, 33]; (3) Laminin (Cat#L9393, Sigma); (4) eMHC (Cat# ab49461, Abcam); (5) MyoD (Cat#IMG132, Imgenex); (6) Pax7 (Cat# ab34360, Abcam); (7) β‐Catenin (Cat# 18‐272‐ 196288, Genway).

    Techniques: Western Blot, Control, Immunodetection, Fluorescence, Microscopy

    Fig. 2 Combined deletion of MuRF1 and MuRF2 causes deficient skeletal muscle regeneration. TA muscles from WT (a and e), from MuRF1 KOs (b and f), MuRF2 KOs (c and g), or from MuRF1&2 dKOs (d and h) were CTX injured and histologically analyzed 3 or 10 days later, respectively. We also histologically analyzed WT and MuRF1&2 dKO mice at 28 days (i and j respectively) after CTX. TA from MuRF1&2 dKO mice presented indications of defective regeneration in all time points analyzed (d, h and j, see text for detailed description). Bar, 20µm. (k) Average density of necrotic fibers in WT and MuRF1&2 dKO 24h after CTX injury; error bars indicate standard deviations (N=3)

    Journal: JCSM Rapid Communications

    Article Title: MuRF1 and MuRF2 are key players in skeletal muscle regeneration involving myogenic deficit and deregulation of the chromatin-remodeling complex

    doi: 10.1002/j.2617-1619.2019.tb00010.x

    Figure Lengend Snippet: Fig. 2 Combined deletion of MuRF1 and MuRF2 causes deficient skeletal muscle regeneration. TA muscles from WT (a and e), from MuRF1 KOs (b and f), MuRF2 KOs (c and g), or from MuRF1&2 dKOs (d and h) were CTX injured and histologically analyzed 3 or 10 days later, respectively. We also histologically analyzed WT and MuRF1&2 dKO mice at 28 days (i and j respectively) after CTX. TA from MuRF1&2 dKO mice presented indications of defective regeneration in all time points analyzed (d, h and j, see text for detailed description). Bar, 20µm. (k) Average density of necrotic fibers in WT and MuRF1&2 dKO 24h after CTX injury; error bars indicate standard deviations (N=3)

    Article Snippet: The primary antibodies used for immunofluorescence were: (1) MuRF1 and (2) MuRF2 [27, 32, 33]; (3) Laminin (Cat#L9393, Sigma); (4) eMHC (Cat# ab49461, Abcam); (5) MyoD (Cat#IMG132, Imgenex); (6) Pax7 (Cat# ab34360, Abcam); (7) β‐Catenin (Cat# 18‐272‐ 196288, Genway).

    Techniques: Muscles

    Fig.3 Simultaneous deletion of MuRF1 and MuRF2 decreases the number of cells positive to Pax7 and Myod. TA muscles from WT, or MuRF1&2 dKO mice were investigated by immunofluorescence 3 (a‐d and j‐m) or 10 days (e‐h and n‐q) after CTX injections. Immunolocalization and percentage of positive eMHC positive myofibers was also determined (u). DAPI (blue), Pax7 and Myod (red), laminin (green) and eMHC (green). Images were obtained with a fluorescence microscope and a 40x air medium objective. Large bar, 50 µm, small bar 10 µm

    Journal: JCSM Rapid Communications

    Article Title: MuRF1 and MuRF2 are key players in skeletal muscle regeneration involving myogenic deficit and deregulation of the chromatin-remodeling complex

    doi: 10.1002/j.2617-1619.2019.tb00010.x

    Figure Lengend Snippet: Fig.3 Simultaneous deletion of MuRF1 and MuRF2 decreases the number of cells positive to Pax7 and Myod. TA muscles from WT, or MuRF1&2 dKO mice were investigated by immunofluorescence 3 (a‐d and j‐m) or 10 days (e‐h and n‐q) after CTX injections. Immunolocalization and percentage of positive eMHC positive myofibers was also determined (u). DAPI (blue), Pax7 and Myod (red), laminin (green) and eMHC (green). Images were obtained with a fluorescence microscope and a 40x air medium objective. Large bar, 50 µm, small bar 10 µm

    Article Snippet: The primary antibodies used for immunofluorescence were: (1) MuRF1 and (2) MuRF2 [27, 32, 33]; (3) Laminin (Cat#L9393, Sigma); (4) eMHC (Cat# ab49461, Abcam); (5) MyoD (Cat#IMG132, Imgenex); (6) Pax7 (Cat# ab34360, Abcam); (7) β‐Catenin (Cat# 18‐272‐ 196288, Genway).

    Techniques: Muscles, Immunofluorescence, Fluorescence, Microscopy

    Fig. 4 Simultaneous deletion of MuRF1 and MuRF2 causes decreased protein expression of myogenic factors and increased apoptosis. (a) Western blots for Myogenin, Myf‐5, FHL2, MARP2 and GAPDH in TA of MuRF1&2 dKO animals 3 and 10 days after CTX injury and silver staining showing even protein loading. Fluorescence images showing apoptotic nuclei by TUNEL assay in WT (b‐d and h‐j) and MuRF1&2 dKO (e‐g and k‐m) muscles 3 (b‐g) and 10 (h‐ m) days after CTX injury. Images were obtained with a fluorescence microscope and a 40x air medium objective. Bar, 30 µm. (n) Percentage of apoptotic nuclei in WT and MuRF1&2 dKO muscles 3 and 10 days after CTX injury

    Journal: JCSM Rapid Communications

    Article Title: MuRF1 and MuRF2 are key players in skeletal muscle regeneration involving myogenic deficit and deregulation of the chromatin-remodeling complex

    doi: 10.1002/j.2617-1619.2019.tb00010.x

    Figure Lengend Snippet: Fig. 4 Simultaneous deletion of MuRF1 and MuRF2 causes decreased protein expression of myogenic factors and increased apoptosis. (a) Western blots for Myogenin, Myf‐5, FHL2, MARP2 and GAPDH in TA of MuRF1&2 dKO animals 3 and 10 days after CTX injury and silver staining showing even protein loading. Fluorescence images showing apoptotic nuclei by TUNEL assay in WT (b‐d and h‐j) and MuRF1&2 dKO (e‐g and k‐m) muscles 3 (b‐g) and 10 (h‐ m) days after CTX injury. Images were obtained with a fluorescence microscope and a 40x air medium objective. Bar, 30 µm. (n) Percentage of apoptotic nuclei in WT and MuRF1&2 dKO muscles 3 and 10 days after CTX injury

    Article Snippet: The primary antibodies used for immunofluorescence were: (1) MuRF1 and (2) MuRF2 [27, 32, 33]; (3) Laminin (Cat#L9393, Sigma); (4) eMHC (Cat# ab49461, Abcam); (5) MyoD (Cat#IMG132, Imgenex); (6) Pax7 (Cat# ab34360, Abcam); (7) β‐Catenin (Cat# 18‐272‐ 196288, Genway).

    Techniques: Expressing, Western Blot, Silver Staining, Fluorescence, TUNEL Assay, Muscles, Microscopy

    Fig. 5 Simultaneous deletion of MuRF1 and MuRF2 time‐shifts the localization/expression of β‐catenin during regeneration. TA muscles from WT (a‐e and k‐o), or MuRF1&2 dKO mice (f‐j and p‐t) were studied by immunofluorescence 3 (a‐j) or 10 days (k‐t) after CTX injections. DAPI (blue), β‐catenin (red), MyoD (green) and laminin (white). Arrows indicate nuclei simultaneously positive to MyoD, B‐catenin and Dapi. Arrow heads indicate non‐nuclear β‐catenin labeling. Images were obtained with a fluorescence microscope and a 40x air medium objective. Bar, 20 µm. (u) Number of β‐catenin positive cells/mm 2 in WT and MuRF1&2 dKO TA muscles. ***p<0.001 vs WT

    Journal: JCSM Rapid Communications

    Article Title: MuRF1 and MuRF2 are key players in skeletal muscle regeneration involving myogenic deficit and deregulation of the chromatin-remodeling complex

    doi: 10.1002/j.2617-1619.2019.tb00010.x

    Figure Lengend Snippet: Fig. 5 Simultaneous deletion of MuRF1 and MuRF2 time‐shifts the localization/expression of β‐catenin during regeneration. TA muscles from WT (a‐e and k‐o), or MuRF1&2 dKO mice (f‐j and p‐t) were studied by immunofluorescence 3 (a‐j) or 10 days (k‐t) after CTX injections. DAPI (blue), β‐catenin (red), MyoD (green) and laminin (white). Arrows indicate nuclei simultaneously positive to MyoD, B‐catenin and Dapi. Arrow heads indicate non‐nuclear β‐catenin labeling. Images were obtained with a fluorescence microscope and a 40x air medium objective. Bar, 20 µm. (u) Number of β‐catenin positive cells/mm 2 in WT and MuRF1&2 dKO TA muscles. ***p<0.001 vs WT

    Article Snippet: The primary antibodies used for immunofluorescence were: (1) MuRF1 and (2) MuRF2 [27, 32, 33]; (3) Laminin (Cat#L9393, Sigma); (4) eMHC (Cat# ab49461, Abcam); (5) MyoD (Cat#IMG132, Imgenex); (6) Pax7 (Cat# ab34360, Abcam); (7) β‐Catenin (Cat# 18‐272‐ 196288, Genway).

    Techniques: Expressing, Muscles, Immunofluorescence, Labeling, Fluorescence, Microscopy

    Fig. 6 siRNA knock down of MuRF1 and MuRF2 reduce myogenesis. (a‐d) Phase contrast micrographs of primary myoblast culture 2 days after induction of differentiation. Images were taken with a 4x objective. Cells were siRNA knocked down for MuRF1 (b), MuRF2 (c) and MuRF1 and MuRF2 combined (d). (a) Arrowheads indicate the normal differentiation pattern generating myotubes. (b‐d) Arrows indicate a severe differentiation deficit. (e) Fusion index of siRNA knocked down cells. (f) Myotube area of siRNA knocked down cells. (g) Number of myotube by field of siRNA knocked down cells. The fusion index was calculated as the ratio of the nuclei number in myotubes with two or more nuclei versus the total number of nuclei. Ten representative images per sample were scored for myotube number and area occupied by myotubes relative to the total area ( a p<0.05 vs Control). Fluorescence images showing reduced expression of eMHC after siRNA knock down for MuRF1 (k‐m) MuRF2 (n‐p) and MuRF1 and MuRF2 combined (q‐s) compared to control (h‐j). Images were obtained with a fluorescence microscope. Bars, 20 µm

    Journal: JCSM Rapid Communications

    Article Title: MuRF1 and MuRF2 are key players in skeletal muscle regeneration involving myogenic deficit and deregulation of the chromatin-remodeling complex

    doi: 10.1002/j.2617-1619.2019.tb00010.x

    Figure Lengend Snippet: Fig. 6 siRNA knock down of MuRF1 and MuRF2 reduce myogenesis. (a‐d) Phase contrast micrographs of primary myoblast culture 2 days after induction of differentiation. Images were taken with a 4x objective. Cells were siRNA knocked down for MuRF1 (b), MuRF2 (c) and MuRF1 and MuRF2 combined (d). (a) Arrowheads indicate the normal differentiation pattern generating myotubes. (b‐d) Arrows indicate a severe differentiation deficit. (e) Fusion index of siRNA knocked down cells. (f) Myotube area of siRNA knocked down cells. (g) Number of myotube by field of siRNA knocked down cells. The fusion index was calculated as the ratio of the nuclei number in myotubes with two or more nuclei versus the total number of nuclei. Ten representative images per sample were scored for myotube number and area occupied by myotubes relative to the total area ( a p<0.05 vs Control). Fluorescence images showing reduced expression of eMHC after siRNA knock down for MuRF1 (k‐m) MuRF2 (n‐p) and MuRF1 and MuRF2 combined (q‐s) compared to control (h‐j). Images were obtained with a fluorescence microscope. Bars, 20 µm

    Article Snippet: The primary antibodies used for immunofluorescence were: (1) MuRF1 and (2) MuRF2 [27, 32, 33]; (3) Laminin (Cat#L9393, Sigma); (4) eMHC (Cat# ab49461, Abcam); (5) MyoD (Cat#IMG132, Imgenex); (6) Pax7 (Cat# ab34360, Abcam); (7) β‐Catenin (Cat# 18‐272‐ 196288, Genway).

    Techniques: Knockdown, Control, Fluorescence, Expressing, Microscopy

    Fig. 7 siRNA knock down of MuRF1 and MuRF2 reduce MyoD positive cell number. Cells were siRNA knocked down for MuRF1 (e‐h), MuRF2 (i‐l) and MuRF1 and MuRF2 combined (m‐p). Immunoflurescence for Pax7 (red) and MyoD (green) and dapi staining was performed. (q) Percentage of positive nuclei for MyoD. (r) Percentage of positive nuclei for Pax7. (s) Percentage of positive nuclei for Pax7 and MyoD. Ten representative images per group were scored for percentage of positive nuclei (*p<0.05 vs Control). Images were obtained with a fluorescence microscope and a 40x air medium objective. Bar, 30 µm

    Journal: JCSM Rapid Communications

    Article Title: MuRF1 and MuRF2 are key players in skeletal muscle regeneration involving myogenic deficit and deregulation of the chromatin-remodeling complex

    doi: 10.1002/j.2617-1619.2019.tb00010.x

    Figure Lengend Snippet: Fig. 7 siRNA knock down of MuRF1 and MuRF2 reduce MyoD positive cell number. Cells were siRNA knocked down for MuRF1 (e‐h), MuRF2 (i‐l) and MuRF1 and MuRF2 combined (m‐p). Immunoflurescence for Pax7 (red) and MyoD (green) and dapi staining was performed. (q) Percentage of positive nuclei for MyoD. (r) Percentage of positive nuclei for Pax7. (s) Percentage of positive nuclei for Pax7 and MyoD. Ten representative images per group were scored for percentage of positive nuclei (*p<0.05 vs Control). Images were obtained with a fluorescence microscope and a 40x air medium objective. Bar, 30 µm

    Article Snippet: The primary antibodies used for immunofluorescence were: (1) MuRF1 and (2) MuRF2 [27, 32, 33]; (3) Laminin (Cat#L9393, Sigma); (4) eMHC (Cat# ab49461, Abcam); (5) MyoD (Cat#IMG132, Imgenex); (6) Pax7 (Cat# ab34360, Abcam); (7) β‐Catenin (Cat# 18‐272‐ 196288, Genway).

    Techniques: Knockdown, Staining, Control, Fluorescence, Microscopy

    Fig. 8 siRNA knock down of MuRF1 and MuRF2 induce accumulation of BAF57 in the nucleus of primary myoblasts culture 2 days after induction of differentiation. (a‐j) Immunolocalization of BAF57 in cells siRNA knocked down for MuRF1 (c and d), MuRF2 (e and f) and MuRF1 and MuRF2 combined (g and h). (i) Representative immunoblots for BAF57 and GAPDH in cytoplasmic fraction from cells siRNA knocked down for MuRF1 (MuRF1 RNAi), MuRF2 (MuRF2 RNAi) and MuRF1 and MuRF2 combined (MuRF1/2 RNAi). (j) Representative immunoblots for BAF57 and GAPDH in nuclear fraction from cells siRNA knocked down for MuRF1 (MuRF1 RNAi), MuRF2 (MuRF2 RNAi) and MuRF1 and MuRF2 combined (MuRF1/2 RNAi). Bar, 40 µm

    Journal: JCSM Rapid Communications

    Article Title: MuRF1 and MuRF2 are key players in skeletal muscle regeneration involving myogenic deficit and deregulation of the chromatin-remodeling complex

    doi: 10.1002/j.2617-1619.2019.tb00010.x

    Figure Lengend Snippet: Fig. 8 siRNA knock down of MuRF1 and MuRF2 induce accumulation of BAF57 in the nucleus of primary myoblasts culture 2 days after induction of differentiation. (a‐j) Immunolocalization of BAF57 in cells siRNA knocked down for MuRF1 (c and d), MuRF2 (e and f) and MuRF1 and MuRF2 combined (g and h). (i) Representative immunoblots for BAF57 and GAPDH in cytoplasmic fraction from cells siRNA knocked down for MuRF1 (MuRF1 RNAi), MuRF2 (MuRF2 RNAi) and MuRF1 and MuRF2 combined (MuRF1/2 RNAi). (j) Representative immunoblots for BAF57 and GAPDH in nuclear fraction from cells siRNA knocked down for MuRF1 (MuRF1 RNAi), MuRF2 (MuRF2 RNAi) and MuRF1 and MuRF2 combined (MuRF1/2 RNAi). Bar, 40 µm

    Article Snippet: The primary antibodies used for immunofluorescence were: (1) MuRF1 and (2) MuRF2 [27, 32, 33]; (3) Laminin (Cat#L9393, Sigma); (4) eMHC (Cat# ab49461, Abcam); (5) MyoD (Cat#IMG132, Imgenex); (6) Pax7 (Cat# ab34360, Abcam); (7) β‐Catenin (Cat# 18‐272‐ 196288, Genway).

    Techniques: Knockdown, Western Blot