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Cusabio elisa kits
Elisa Kits, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 2 article reviews
elisa kits - by Bioz Stars, 2026-10
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Related Articles

Enzyme-linked Immunosorbent Assay:

Article Title: Serum proteomics identify biomarkers and pathogenesis of portopulmonary hypertension diagnosed based on echocardiography
Article Snippet: .. We measured the levels of VTN, APOA1, and APOA2 using kits called ELISA kits (VTN: CSB-E08983h; APOA1: CSB-E08103h; APOA2: CSB-E13504h; CUSABIO). ..

Article Title: Serum proteomics identify biomarkers and pathogenesis of portopulmonary hypertension diagnosed based on echocardiography.
Article Snippet: .. Detection methods for VTN, APOA1, and APOA2 levels We measured the levels of VTN, APOA1, and APOA2 using kits called ELISA kits (VTN: CSB-E08983h; APOA1: CSB-E08103h; APOA2: CSB-E13504h; CUSABIO). ..



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a MRI images, changes in AFP, and quantification of tumor volume in representative HCC-resistant patients before and after apatinib treatment. Scale bars, 10 cm. b MRI images, changes in AFP, and quantification of tumor thrombus volume in representative HCC-sensitive patients before and after apatinib treatment. Scale bars, 10 cm. c The GO pathway analysis of differential genes was enriched, with <t>APOA2</t> ranking first in the small molecule metabolic process. d The KEGG pathway analysis of differential genes was enriched, with APOA2 ranking first in the PPAR signaling pathway. e Intensity of APOA2 IHC staining in 10 paired HCC patient tissues (sensitive vs resistant). Scale bars, 50 µm. f Predicted network diagram of the interactions between APOA2 and VEGFR2.
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Verification of transcriptome sequencing results. The representative images and quantitative results of immunohistochemistry staining of integrin subunit alpha L (ITGAL) ( A–B ), integrin subunit alpha M (ITGAM) ( C–D ), integrin subunit alpha D (ITGAD) ( E–F ), integrin subunit beta 3 (ITGB3) ( G–H ), and fibrinogen alpha chain (FGA) ( I–J ) in heart tissues of WT + NC, KO + NC, WT + HF and KO + HF groups of female mice ( n = 6), Scale bars = 50 μm. K–L Representative images and quantitative results of immunofluorescence of fibrinogen beta chain (FGB) in heart tissues of WT + NC, KO + NC, WT + HF and KO + HF groups of female mice ( n = 6), Scale bars = 50 μm. Representative images and quantitative results of immunofluorescence of apolipoprotein A-1 (ApoA1) ( M–N ), apolipoprotein A-2 <t>(ApoA2)</t> ( O–P ), and apolipoprotein B (ApoB) ( Q–R ) in liver tissues of WT + NC, KO + NC, WT + HF and KO + HF groups of female mice ( n = 6), Scale bar = 50 μm. Data are expressed as mean ± SD and one-way ANOVA with Tukey’s test was used for multiple comparisons; ns indicated no significant difference, ** P < 0.01, *** P < 0.001, and **** P < 0.0001
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(A) Congo-red staining in organs of PAI1 −/− mice. Representative images of Congo-red fluorescence in different organs are shown. Lower panel, Congo red birefringency in spleen and kidney of a PAI1 −/− mouse. Scale bars are indicated. (B) Electron micrograph of kidney from a PAI-1 −/− mouse showing amyloid fibrils in the extracellular compartment. Scale bars are indicated. (C) Amyloidosis scores relative to age in organs of PAI-1 −/− mice (n = 6-11 except tongue and intestine, n = 3-5). Protein deposition was graded on a four-point scale: 1, rare localized deposits; 2, frequent localized deposits; 3, deposits throughout the organ; and 4, deposits throughout the organ with visible tissue disorganization. (D) Amyloidosis scores in organs of > 12 months old PAI-1 −/− (n = 17) and C57Bl/6 control mice (n = 28). p < 0.0001 for all organs except intestine p = 0.013 (multiple t-tests, Benjamini–Hochberg FDR correction) (E) Representative immunofluorescence with an anti-mouse <t>APOA2</t> antibody colocalized with Amytracker 680 © in organs of an 18 months old PAI-1 −/− mouse. Scale bars are indicated. (F) Serum APOA2 dosage in PAI-1 −/− (n = 13) and control mice (n = 16). (G) Amyloidosis scores in spleens of 6 months old PAI-1 −/− mice injected (n = 6) or not (n = 7) with AEF at month 3. (H) Urine albumin dosage relative to the amyloid score in spleens of PAI1 −/− mice (n ≥ 4 per score group). In F-H, differences between groups were calculated using a two-tailed Mann-Whitney test (Prism v8 GraphPad). P values are indicated when p < 0.05.
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(A) Congo-red staining in organs of PAI1 −/− mice. Representative images of Congo-red fluorescence in different organs are shown. Lower panel, Congo red birefringency in spleen and kidney of a PAI1 −/− mouse. Scale bars are indicated. (B) Electron micrograph of kidney from a PAI-1 −/− mouse showing amyloid fibrils in the extracellular compartment. Scale bars are indicated. (C) Amyloidosis scores relative to age in organs of PAI-1 −/− mice (n = 6-11 except tongue and intestine, n = 3-5). Protein deposition was graded on a four-point scale: 1, rare localized deposits; 2, frequent localized deposits; 3, deposits throughout the organ; and 4, deposits throughout the organ with visible tissue disorganization. (D) Amyloidosis scores in organs of > 12 months old PAI-1 −/− (n = 17) and C57Bl/6 control mice (n = 28). p < 0.0001 for all organs except intestine p = 0.013 (multiple t-tests, Benjamini–Hochberg FDR correction) (E) Representative immunofluorescence with an anti-mouse <t>APOA2</t> antibody colocalized with Amytracker 680 © in organs of an 18 months old PAI-1 −/− mouse. Scale bars are indicated. (F) Serum APOA2 dosage in PAI-1 −/− (n = 13) and control mice (n = 16). (G) Amyloidosis scores in spleens of 6 months old PAI-1 −/− mice injected (n = 6) or not (n = 7) with AEF at month 3. (H) Urine albumin dosage relative to the amyloid score in spleens of PAI1 −/− mice (n ≥ 4 per score group). In F-H, differences between groups were calculated using a two-tailed Mann-Whitney test (Prism v8 GraphPad). P values are indicated when p < 0.05.
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(A) Congo-red staining in organs of PAI1 −/− mice. Representative images of Congo-red fluorescence in different organs are shown. Lower panel, Congo red birefringency in spleen and kidney of a PAI1 −/− mouse. Scale bars are indicated. (B) Electron micrograph of kidney from a PAI-1 −/− mouse showing amyloid fibrils in the extracellular compartment. Scale bars are indicated. (C) Amyloidosis scores relative to age in organs of PAI-1 −/− mice (n = 6-11 except tongue and intestine, n = 3-5). Protein deposition was graded on a four-point scale: 1, rare localized deposits; 2, frequent localized deposits; 3, deposits throughout the organ; and 4, deposits throughout the organ with visible tissue disorganization. (D) Amyloidosis scores in organs of > 12 months old PAI-1 −/− (n = 17) and C57Bl/6 control mice (n = 28). p < 0.0001 for all organs except intestine p = 0.013 (multiple t-tests, Benjamini–Hochberg FDR correction) (E) Representative immunofluorescence with an anti-mouse <t>APOA2</t> antibody colocalized with Amytracker 680 © in organs of an 18 months old PAI-1 −/− mouse. Scale bars are indicated. (F) Serum APOA2 dosage in PAI-1 −/− (n = 13) and control mice (n = 16). (G) Amyloidosis scores in spleens of 6 months old PAI-1 −/− mice injected (n = 6) or not (n = 7) with AEF at month 3. (H) Urine albumin dosage relative to the amyloid score in spleens of PAI1 −/− mice (n ≥ 4 per score group). In F-H, differences between groups were calculated using a two-tailed Mann-Whitney test (Prism v8 GraphPad). P values are indicated when p < 0.05.
Elisa Kits, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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(A) Congo-red staining in organs of PAI1 −/− mice. Representative images of Congo-red fluorescence in different organs are shown. Lower panel, Congo red birefringency in spleen and kidney of a PAI1 −/− mouse. Scale bars are indicated. (B) Electron micrograph of kidney from a PAI-1 −/− mouse showing amyloid fibrils in the extracellular compartment. Scale bars are indicated. (C) Amyloidosis scores relative to age in organs of PAI-1 −/− mice (n = 6-11 except tongue and intestine, n = 3-5). Protein deposition was graded on a four-point scale: 1, rare localized deposits; 2, frequent localized deposits; 3, deposits throughout the organ; and 4, deposits throughout the organ with visible tissue disorganization. (D) Amyloidosis scores in organs of > 12 months old PAI-1 −/− (n = 17) and C57Bl/6 control mice (n = 28). p < 0.0001 for all organs except intestine p = 0.013 (multiple t-tests, Benjamini–Hochberg FDR correction) (E) Representative immunofluorescence with an anti-mouse <t>APOA2</t> antibody colocalized with Amytracker 680 © in organs of an 18 months old PAI-1 −/− mouse. Scale bars are indicated. (F) Serum APOA2 dosage in PAI-1 −/− (n = 13) and control mice (n = 16). (G) Amyloidosis scores in spleens of 6 months old PAI-1 −/− mice injected (n = 6) or not (n = 7) with AEF at month 3. (H) Urine albumin dosage relative to the amyloid score in spleens of PAI1 −/− mice (n ≥ 4 per score group). In F-H, differences between groups were calculated using a two-tailed Mann-Whitney test (Prism v8 GraphPad). P values are indicated when p < 0.05.
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(A) Congo-red staining in organs of PAI1 −/− mice. Representative images of Congo-red fluorescence in different organs are shown. Lower panel, Congo red birefringency in spleen and kidney of a PAI1 −/− mouse. Scale bars are indicated. (B) Electron micrograph of kidney from a PAI-1 −/− mouse showing amyloid fibrils in the extracellular compartment. Scale bars are indicated. (C) Amyloidosis scores relative to age in organs of PAI-1 −/− mice (n = 6-11 except tongue and intestine, n = 3-5). Protein deposition was graded on a four-point scale: 1, rare localized deposits; 2, frequent localized deposits; 3, deposits throughout the organ; and 4, deposits throughout the organ with visible tissue disorganization. (D) Amyloidosis scores in organs of > 12 months old PAI-1 −/− (n = 17) and C57Bl/6 control mice (n = 28). p < 0.0001 for all organs except intestine p = 0.013 (multiple t-tests, Benjamini–Hochberg FDR correction) (E) Representative immunofluorescence with an anti-mouse <t>APOA2</t> antibody colocalized with Amytracker 680 © in organs of an 18 months old PAI-1 −/− mouse. Scale bars are indicated. (F) Serum APOA2 dosage in PAI-1 −/− (n = 13) and control mice (n = 16). (G) Amyloidosis scores in spleens of 6 months old PAI-1 −/− mice injected (n = 6) or not (n = 7) with AEF at month 3. (H) Urine albumin dosage relative to the amyloid score in spleens of PAI1 −/− mice (n ≥ 4 per score group). In F-H, differences between groups were calculated using a two-tailed Mann-Whitney test (Prism v8 GraphPad). P values are indicated when p < 0.05.
Apoa2, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


a MRI images, changes in AFP, and quantification of tumor volume in representative HCC-resistant patients before and after apatinib treatment. Scale bars, 10 cm. b MRI images, changes in AFP, and quantification of tumor thrombus volume in representative HCC-sensitive patients before and after apatinib treatment. Scale bars, 10 cm. c The GO pathway analysis of differential genes was enriched, with APOA2 ranking first in the small molecule metabolic process. d The KEGG pathway analysis of differential genes was enriched, with APOA2 ranking first in the PPAR signaling pathway. e Intensity of APOA2 IHC staining in 10 paired HCC patient tissues (sensitive vs resistant). Scale bars, 50 µm. f Predicted network diagram of the interactions between APOA2 and VEGFR2.

Journal: Cell Death Discovery

Article Title: APOA2-mediated endothelial mesenchymal transition and cancer lipid metabolism reprogramming confers antiangiogenic drug resistance through TGF-β

doi: 10.1038/s41420-026-02984-5

Figure Lengend Snippet: a MRI images, changes in AFP, and quantification of tumor volume in representative HCC-resistant patients before and after apatinib treatment. Scale bars, 10 cm. b MRI images, changes in AFP, and quantification of tumor thrombus volume in representative HCC-sensitive patients before and after apatinib treatment. Scale bars, 10 cm. c The GO pathway analysis of differential genes was enriched, with APOA2 ranking first in the small molecule metabolic process. d The KEGG pathway analysis of differential genes was enriched, with APOA2 ranking first in the PPAR signaling pathway. e Intensity of APOA2 IHC staining in 10 paired HCC patient tissues (sensitive vs resistant). Scale bars, 50 µm. f Predicted network diagram of the interactions between APOA2 and VEGFR2.

Article Snippet: Primary APOA2 antibody (Proteintech, 16845-1-AP, CHN) was diluted at 1:50, while mouse/rabbit linker (Santa Cruz, sc2357, USA) was diluted at 1:100.

Techniques: Immunohistochemistry

After the evaluation of acquired drug resistance, the HCC-bearing mice were divided into 3 groups: (C)control ( n = 7), (R)resistant ( n = 7), and (S)sensitive ( n = 24). a Quantification of subcutaneous tumor mass and volume in the three groups. Numbers 1–7 represent control group, 1–7 for resistance group, and 1–7 for sensitivity group. * p < 0.05, ns, not significant. b . Representative images of CD31 immunofluorescence staining of tumor tissue. The upper part of the image is a comprehensive view of CD31 staining of the entire tumor tissue section, while the bottom part shows CD31 staining under magnification. CD31 + microvessel signals were randomly quantified from 12 fields ( n = 7 mice in each group), Scale bars, 50 µm. * p < 0.05, ns, not significant. c and d . Western blotting of APOA2, VEGFR2, and P-VEGFR2 in tumor tissue ( n = 4). e Representative images of APOA2 IHC staining intensity of tumor tissue, Scale bars, 100 µm. The upper part of the image is a comprehensive view of APOA2 staining of the entire tumor tissue section, while the bottom part shows APOA2 staining under magnification. Scale bars, 100 µm. * p < 0.05, ns, not significant.

Journal: Cell Death Discovery

Article Title: APOA2-mediated endothelial mesenchymal transition and cancer lipid metabolism reprogramming confers antiangiogenic drug resistance through TGF-β

doi: 10.1038/s41420-026-02984-5

Figure Lengend Snippet: After the evaluation of acquired drug resistance, the HCC-bearing mice were divided into 3 groups: (C)control ( n = 7), (R)resistant ( n = 7), and (S)sensitive ( n = 24). a Quantification of subcutaneous tumor mass and volume in the three groups. Numbers 1–7 represent control group, 1–7 for resistance group, and 1–7 for sensitivity group. * p < 0.05, ns, not significant. b . Representative images of CD31 immunofluorescence staining of tumor tissue. The upper part of the image is a comprehensive view of CD31 staining of the entire tumor tissue section, while the bottom part shows CD31 staining under magnification. CD31 + microvessel signals were randomly quantified from 12 fields ( n = 7 mice in each group), Scale bars, 50 µm. * p < 0.05, ns, not significant. c and d . Western blotting of APOA2, VEGFR2, and P-VEGFR2 in tumor tissue ( n = 4). e Representative images of APOA2 IHC staining intensity of tumor tissue, Scale bars, 100 µm. The upper part of the image is a comprehensive view of APOA2 staining of the entire tumor tissue section, while the bottom part shows APOA2 staining under magnification. Scale bars, 100 µm. * p < 0.05, ns, not significant.

Article Snippet: Primary APOA2 antibody (Proteintech, 16845-1-AP, CHN) was diluted at 1:50, while mouse/rabbit linker (Santa Cruz, sc2357, USA) was diluted at 1:100.

Techniques: Control, Immunofluorescence, Staining, Western Blot, Immunohistochemistry

a Representative images of HCC cell lines overexpressing APOA2. Scale bars, 100 µm. Western blotting verified the protein levels of APOA2, VEGFR2, and P-VEGFR2 in 4 cell lines. b – d Subcutaneous tumor, tumor volume and tumor mass quantification, along with tumor growth curve of each group ( n = 6). e – g Characterization of tumor inhibition rate in each group. *** p < 0.001, **** p < 0.0001, ns not significant.

Journal: Cell Death Discovery

Article Title: APOA2-mediated endothelial mesenchymal transition and cancer lipid metabolism reprogramming confers antiangiogenic drug resistance through TGF-β

doi: 10.1038/s41420-026-02984-5

Figure Lengend Snippet: a Representative images of HCC cell lines overexpressing APOA2. Scale bars, 100 µm. Western blotting verified the protein levels of APOA2, VEGFR2, and P-VEGFR2 in 4 cell lines. b – d Subcutaneous tumor, tumor volume and tumor mass quantification, along with tumor growth curve of each group ( n = 6). e – g Characterization of tumor inhibition rate in each group. *** p < 0.001, **** p < 0.0001, ns not significant.

Article Snippet: Primary APOA2 antibody (Proteintech, 16845-1-AP, CHN) was diluted at 1:50, while mouse/rabbit linker (Santa Cruz, sc2357, USA) was diluted at 1:100.

Techniques: Western Blot, Inhibition

a – f The experiment comprised two groups: control (Control) and APOA2 overexpression (APOA2). a , d Colony formation assay conducted on MHCC97H and SMMC7721 cells ( n = 3), b , e Representative images from EdU assay performed on MHCC97H and SMMC7721 cells, with EdU signals quantified from 12 fields ( n = 6), Scale bars, 50 µm. c , f CCK8 assay results of MHCC97H and SMMC7721 cells. g The experiment comprised 4 groups: control group receiving solvent and apatinib (Control + Vehicle vs Control + Apatinib), and the APOA2 overexpression group receiving solvent and apatinib (APOA2+Vehicle vs APOA2+Apatinib). Representative images of Ki67 and cleaved-caspase 3 immunofluorescence staining of tumor tissue, with Ki67+ and cleaved-caspase 3+ signals quantified from 12 fields ( n = 6). Scale bars, 100 µm. * p < 0.05, ns not significant.

Journal: Cell Death Discovery

Article Title: APOA2-mediated endothelial mesenchymal transition and cancer lipid metabolism reprogramming confers antiangiogenic drug resistance through TGF-β

doi: 10.1038/s41420-026-02984-5

Figure Lengend Snippet: a – f The experiment comprised two groups: control (Control) and APOA2 overexpression (APOA2). a , d Colony formation assay conducted on MHCC97H and SMMC7721 cells ( n = 3), b , e Representative images from EdU assay performed on MHCC97H and SMMC7721 cells, with EdU signals quantified from 12 fields ( n = 6), Scale bars, 50 µm. c , f CCK8 assay results of MHCC97H and SMMC7721 cells. g The experiment comprised 4 groups: control group receiving solvent and apatinib (Control + Vehicle vs Control + Apatinib), and the APOA2 overexpression group receiving solvent and apatinib (APOA2+Vehicle vs APOA2+Apatinib). Representative images of Ki67 and cleaved-caspase 3 immunofluorescence staining of tumor tissue, with Ki67+ and cleaved-caspase 3+ signals quantified from 12 fields ( n = 6). Scale bars, 100 µm. * p < 0.05, ns not significant.

Article Snippet: Primary APOA2 antibody (Proteintech, 16845-1-AP, CHN) was diluted at 1:50, while mouse/rabbit linker (Santa Cruz, sc2357, USA) was diluted at 1:100.

Techniques: Control, Over Expression, Colony Assay, EdU Assay, CCK-8 Assay, Solvent, Immunofluorescence, Staining

a Representative bright-field images of tubular formation in HUVECs cultured with conditioned media from MHCC97H and SMCC7721 (overexpressing APOA2 or not). Scale bar, 400 µm. b Representative images of EdU assay conducted on HUVECs cultured with conditioned media from MHCC97H and SMCC7721 (overexpressing APOA2 or not), with EdU signals quantified from 12 fields ( n = 6). Scale bars, 100 µm. c Representative images of migration of HUVECs cultured with conditioned media from MHCC97H and SMCC7721 (overexpressing APOA2 or not), Scale bars, 100 µm. * p < 0.05, ns not significant.

Journal: Cell Death Discovery

Article Title: APOA2-mediated endothelial mesenchymal transition and cancer lipid metabolism reprogramming confers antiangiogenic drug resistance through TGF-β

doi: 10.1038/s41420-026-02984-5

Figure Lengend Snippet: a Representative bright-field images of tubular formation in HUVECs cultured with conditioned media from MHCC97H and SMCC7721 (overexpressing APOA2 or not). Scale bar, 400 µm. b Representative images of EdU assay conducted on HUVECs cultured with conditioned media from MHCC97H and SMCC7721 (overexpressing APOA2 or not), with EdU signals quantified from 12 fields ( n = 6). Scale bars, 100 µm. c Representative images of migration of HUVECs cultured with conditioned media from MHCC97H and SMCC7721 (overexpressing APOA2 or not), Scale bars, 100 µm. * p < 0.05, ns not significant.

Article Snippet: Primary APOA2 antibody (Proteintech, 16845-1-AP, CHN) was diluted at 1:50, while mouse/rabbit linker (Santa Cruz, sc2357, USA) was diluted at 1:100.

Techniques: Cell Culture, EdU Assay, Migration

a Volcano plot of differentially expressed proteins between the APOA2 overexpression group and the control group, with a fold change ≥ 1.5 and adjusted p < 0.01 ( n = 3). Gray denotes no significant difference, blue indicates low expression, and red indicates high expression. The volcano plot labels the five highest expressed proteins and five lowest expressed proteins. b Histogram of 5 highest expressed proteins and 5 lowest expressed proteins ( n = 3). c Enrichment analysis of KEGG pathways for differentially expressed proteins between the APOA2 overexpression group and the control group. d Histogram showing levels of TGF-β ligand, receptor, and signaling pathway-related protein in proteomics (n = 3). e Pearson correlation analysis of five highly expressed proteins and TGF-β in HCC. f Relative mRNA levels of TGF-β in HCC cells and tumor tissues with or without overexpressing APOA2 analyzed by real-time quantitative PCR ( n = 6). g ELISA detection of TGF-β in HCC cell (with or without overexpressing APOA2) medium and serum of HCC-bearing mice (with or without overexpressing APOA2). h Western blotting detecting the protein levels of TGF-βR1, TGF-βR2, P-TGFβR1 and P-TGFβR2 in HCC cells and tumor tissues with or without overexpressing APOA2. * p < 0.05, ns, not significant.

Journal: Cell Death Discovery

Article Title: APOA2-mediated endothelial mesenchymal transition and cancer lipid metabolism reprogramming confers antiangiogenic drug resistance through TGF-β

doi: 10.1038/s41420-026-02984-5

Figure Lengend Snippet: a Volcano plot of differentially expressed proteins between the APOA2 overexpression group and the control group, with a fold change ≥ 1.5 and adjusted p < 0.01 ( n = 3). Gray denotes no significant difference, blue indicates low expression, and red indicates high expression. The volcano plot labels the five highest expressed proteins and five lowest expressed proteins. b Histogram of 5 highest expressed proteins and 5 lowest expressed proteins ( n = 3). c Enrichment analysis of KEGG pathways for differentially expressed proteins between the APOA2 overexpression group and the control group. d Histogram showing levels of TGF-β ligand, receptor, and signaling pathway-related protein in proteomics (n = 3). e Pearson correlation analysis of five highly expressed proteins and TGF-β in HCC. f Relative mRNA levels of TGF-β in HCC cells and tumor tissues with or without overexpressing APOA2 analyzed by real-time quantitative PCR ( n = 6). g ELISA detection of TGF-β in HCC cell (with or without overexpressing APOA2) medium and serum of HCC-bearing mice (with or without overexpressing APOA2). h Western blotting detecting the protein levels of TGF-βR1, TGF-βR2, P-TGFβR1 and P-TGFβR2 in HCC cells and tumor tissues with or without overexpressing APOA2. * p < 0.05, ns, not significant.

Article Snippet: Primary APOA2 antibody (Proteintech, 16845-1-AP, CHN) was diluted at 1:50, while mouse/rabbit linker (Santa Cruz, sc2357, USA) was diluted at 1:100.

Techniques: Over Expression, Control, Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Western Blot

a Enrichment analysis of GO pathways for differentially expressed proteins between APOA2 overexpression and the control group, with a fold change ≥ 1.5 and adjusted p -value < 0.01. b Glucose consumption in MHCC97H cells in the designated group ( n = 6). c Lactate production in MHCC97H cells in the designated group ( n = 6). d Mito Fuel Flex test revealed dependence on the oxidation of glucose, glutamine, or FA in MHCC97H cells in the designated group ( n = 6). e BODIPY-FA uptake in MHCC97H cells in the designated group. f β-oxidation assay in MHCC97H cells in the designated group ( n = 6). g Intracellular ATP levels in MHCC97H cells in the designated group ( n = 6). * p < 0.05, ns not significant.

Journal: Cell Death Discovery

Article Title: APOA2-mediated endothelial mesenchymal transition and cancer lipid metabolism reprogramming confers antiangiogenic drug resistance through TGF-β

doi: 10.1038/s41420-026-02984-5

Figure Lengend Snippet: a Enrichment analysis of GO pathways for differentially expressed proteins between APOA2 overexpression and the control group, with a fold change ≥ 1.5 and adjusted p -value < 0.01. b Glucose consumption in MHCC97H cells in the designated group ( n = 6). c Lactate production in MHCC97H cells in the designated group ( n = 6). d Mito Fuel Flex test revealed dependence on the oxidation of glucose, glutamine, or FA in MHCC97H cells in the designated group ( n = 6). e BODIPY-FA uptake in MHCC97H cells in the designated group. f β-oxidation assay in MHCC97H cells in the designated group ( n = 6). g Intracellular ATP levels in MHCC97H cells in the designated group ( n = 6). * p < 0.05, ns not significant.

Article Snippet: Primary APOA2 antibody (Proteintech, 16845-1-AP, CHN) was diluted at 1:50, while mouse/rabbit linker (Santa Cruz, sc2357, USA) was diluted at 1:100.

Techniques: Over Expression, Control, Oxidation Assay

Verification of transcriptome sequencing results. The representative images and quantitative results of immunohistochemistry staining of integrin subunit alpha L (ITGAL) ( A–B ), integrin subunit alpha M (ITGAM) ( C–D ), integrin subunit alpha D (ITGAD) ( E–F ), integrin subunit beta 3 (ITGB3) ( G–H ), and fibrinogen alpha chain (FGA) ( I–J ) in heart tissues of WT + NC, KO + NC, WT + HF and KO + HF groups of female mice ( n = 6), Scale bars = 50 μm. K–L Representative images and quantitative results of immunofluorescence of fibrinogen beta chain (FGB) in heart tissues of WT + NC, KO + NC, WT + HF and KO + HF groups of female mice ( n = 6), Scale bars = 50 μm. Representative images and quantitative results of immunofluorescence of apolipoprotein A-1 (ApoA1) ( M–N ), apolipoprotein A-2 (ApoA2) ( O–P ), and apolipoprotein B (ApoB) ( Q–R ) in liver tissues of WT + NC, KO + NC, WT + HF and KO + HF groups of female mice ( n = 6), Scale bar = 50 μm. Data are expressed as mean ± SD and one-way ANOVA with Tukey’s test was used for multiple comparisons; ns indicated no significant difference, ** P < 0.01, *** P < 0.001, and **** P < 0.0001

Journal: Cardiovascular Diabetology

Article Title: Sex-specific cardioprotective role of miR-30a-5p through estrogen-dependent mechanisms in a mouse model of heart failure

doi: 10.1186/s12933-026-03090-7

Figure Lengend Snippet: Verification of transcriptome sequencing results. The representative images and quantitative results of immunohistochemistry staining of integrin subunit alpha L (ITGAL) ( A–B ), integrin subunit alpha M (ITGAM) ( C–D ), integrin subunit alpha D (ITGAD) ( E–F ), integrin subunit beta 3 (ITGB3) ( G–H ), and fibrinogen alpha chain (FGA) ( I–J ) in heart tissues of WT + NC, KO + NC, WT + HF and KO + HF groups of female mice ( n = 6), Scale bars = 50 μm. K–L Representative images and quantitative results of immunofluorescence of fibrinogen beta chain (FGB) in heart tissues of WT + NC, KO + NC, WT + HF and KO + HF groups of female mice ( n = 6), Scale bars = 50 μm. Representative images and quantitative results of immunofluorescence of apolipoprotein A-1 (ApoA1) ( M–N ), apolipoprotein A-2 (ApoA2) ( O–P ), and apolipoprotein B (ApoB) ( Q–R ) in liver tissues of WT + NC, KO + NC, WT + HF and KO + HF groups of female mice ( n = 6), Scale bar = 50 μm. Data are expressed as mean ± SD and one-way ANOVA with Tukey’s test was used for multiple comparisons; ns indicated no significant difference, ** P < 0.01, *** P < 0.001, and **** P < 0.0001

Article Snippet: For immunofluorescence, sections were incubated with primary antibodies, including APOA1 (Cat#: A24291, Abclonal, Wuhan, China), APOA2 (Cat#: A3321, Abclonal, Wuhan, China), APOB (Cat#: A25420, Abclonal, Wuhan, China), FGB (Cat#: A1401, Abclonal, Wuhan, China), ESRRA (Cat#: A14184, Abclonal, Wuhan, China), and PELP1 (Cat#: A3189, Abclonal, Wuhan, China) respectively.

Techniques: Sequencing, Immunohistochemistry, Staining, Immunofluorescence

(A) Congo-red staining in organs of PAI1 −/− mice. Representative images of Congo-red fluorescence in different organs are shown. Lower panel, Congo red birefringency in spleen and kidney of a PAI1 −/− mouse. Scale bars are indicated. (B) Electron micrograph of kidney from a PAI-1 −/− mouse showing amyloid fibrils in the extracellular compartment. Scale bars are indicated. (C) Amyloidosis scores relative to age in organs of PAI-1 −/− mice (n = 6-11 except tongue and intestine, n = 3-5). Protein deposition was graded on a four-point scale: 1, rare localized deposits; 2, frequent localized deposits; 3, deposits throughout the organ; and 4, deposits throughout the organ with visible tissue disorganization. (D) Amyloidosis scores in organs of > 12 months old PAI-1 −/− (n = 17) and C57Bl/6 control mice (n = 28). p < 0.0001 for all organs except intestine p = 0.013 (multiple t-tests, Benjamini–Hochberg FDR correction) (E) Representative immunofluorescence with an anti-mouse APOA2 antibody colocalized with Amytracker 680 © in organs of an 18 months old PAI-1 −/− mouse. Scale bars are indicated. (F) Serum APOA2 dosage in PAI-1 −/− (n = 13) and control mice (n = 16). (G) Amyloidosis scores in spleens of 6 months old PAI-1 −/− mice injected (n = 6) or not (n = 7) with AEF at month 3. (H) Urine albumin dosage relative to the amyloid score in spleens of PAI1 −/− mice (n ≥ 4 per score group). In F-H, differences between groups were calculated using a two-tailed Mann-Whitney test (Prism v8 GraphPad). P values are indicated when p < 0.05.

Journal: bioRxiv

Article Title: Accelerated APOA-II senile amyloidosis in a PAI-1 (plasminogen activator inhibitor 1) knock-out model

doi: 10.64898/2025.12.18.695159

Figure Lengend Snippet: (A) Congo-red staining in organs of PAI1 −/− mice. Representative images of Congo-red fluorescence in different organs are shown. Lower panel, Congo red birefringency in spleen and kidney of a PAI1 −/− mouse. Scale bars are indicated. (B) Electron micrograph of kidney from a PAI-1 −/− mouse showing amyloid fibrils in the extracellular compartment. Scale bars are indicated. (C) Amyloidosis scores relative to age in organs of PAI-1 −/− mice (n = 6-11 except tongue and intestine, n = 3-5). Protein deposition was graded on a four-point scale: 1, rare localized deposits; 2, frequent localized deposits; 3, deposits throughout the organ; and 4, deposits throughout the organ with visible tissue disorganization. (D) Amyloidosis scores in organs of > 12 months old PAI-1 −/− (n = 17) and C57Bl/6 control mice (n = 28). p < 0.0001 for all organs except intestine p = 0.013 (multiple t-tests, Benjamini–Hochberg FDR correction) (E) Representative immunofluorescence with an anti-mouse APOA2 antibody colocalized with Amytracker 680 © in organs of an 18 months old PAI-1 −/− mouse. Scale bars are indicated. (F) Serum APOA2 dosage in PAI-1 −/− (n = 13) and control mice (n = 16). (G) Amyloidosis scores in spleens of 6 months old PAI-1 −/− mice injected (n = 6) or not (n = 7) with AEF at month 3. (H) Urine albumin dosage relative to the amyloid score in spleens of PAI1 −/− mice (n ≥ 4 per score group). In F-H, differences between groups were calculated using a two-tailed Mann-Whitney test (Prism v8 GraphPad). P values are indicated when p < 0.05.

Article Snippet: Western blotting of purified fibrils with a rabbit polyclonal anti-mouse APOA2 (ABClonal #A14690) revealed by an anti-rabbit IgG-HRP (cell signaling #7074P2) showed a major band at ~8 kDa ( Supplementary Figure 1B ) and MS identified peptides covering the full length secreted APOA2 protein as the main constituent of the deposits, including the propeptide known to be highly amyloidogenic ( Supplementary Figure 1C ) [ ].

Techniques: Staining, Fluorescence, Control, Immunofluorescence, Injection, Two Tailed Test, MANN-WHITNEY