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anti phospho p66 ser36 antibody  (Bioss)


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    Structured Review

    Bioss anti phospho p66 ser36 antibody
    Anti Phospho P66 Ser36 Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/shc(ser36)+polyclonal+antibody/SHC(Ser36)+Polyclonal+Antibody/pm34719845-40-4-12
    Average 92 stars, based on 3 article reviews
    anti phospho p66 ser36 antibody - by Bioz Stars, 2026-09
    92/100 stars

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    Related Articles

    Staining:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    Transfection:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    Fluorescence:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    TUNEL Assay:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    Incubation:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    Binding Assay:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    Expressing:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    Mutagenesis:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    Luciferase:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    Construct:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.

    Activity Assay:

    Article Title: Genistein suppresses ox-LDL-elicited oxidative stress and senescence in HUVECs through the SIRT1-p66shc-Foxo3a pathways.
    Article Snippet: Funding information Natural Science Foundation of Shanxi Province, Grant/Award Number: 201801D121317 Abstract The anti‐senescence function of genistein is related to inhibiting oxidative stress, however, the mechanism has not been clarified.. The present study aimed to explore the effects of genistein on oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial senescence and the role of the sirtuin‐1 (SIRT1)—66‐kDa Src homology 2 domain‐containing protein (p66Shc)–forkhead box protein O3 (Foxo3a) pathways in the process.. In this paper, human umbilical vein endothelial cells were pretreated with 1000 nM genistein for 30min and then incubated with 50mg/L ox‐LDL for another 12 h; meanwhile, the functions of adenovirus‐mediated overexpression of p66shc and small interfering RNA‐mediated silencing of SIRT1 were investigated.



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    anti phospho p66 ser36 antibody  (Bioss)
    92
    Bioss anti phospho p66 ser36 antibody
    Anti Phospho P66 Ser36 Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/shc(ser36)+polyclonal+antibody/SHC(Ser36)+Polyclonal+Antibody/pm34719845-40-4-12
    Average 92 stars, based on 1 article reviews
    anti phospho p66 ser36 antibody - by Bioz Stars, 2026-09
    92/100 stars
    		  Buy from Supplier
    p p66shc  (Bioss)
    92
    Bioss p p66shc
    <t>p66Shc</t> silencing was induced via lentiviruses delivered to C57BL/6 mice exposed to APAP (300 mg/kg). a , b Liver p66Shc, p52Shc, and p46Shc protein, n = 3. ** p < 0.01 vs. the control group. c Serum ALT levels, n = 8. d Serum AST levels, n = 8. e H&E staining. Scale bar, 200 μm. f , g Mitochondrial dynamics perturbation was determined via TEM (×2000/×10,000, magnification, red arrow). h Liver H 2 O 2 levels, n = 8. i Liver GSH levels, n = 8. j Liver MDA levels, n = 8. k , l Liver p66Shc, p-p66Shc, OMA1, L-OPA1, S-OPA1, MFN2, DRP1, p-DRP1 protein, n = 3. m , n Liver OMA1 ubiquitination level, n = 3. * p < 0.05, ** p < 0.01 vs. the LV-control group; # p < 0.05, ## p < 0.01 vs. the APAP group.
    P P66shc, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/shc(ser36)+polyclonal+antibody/SHC(Ser36)+Polyclonal+Antibody/pmc07648761-57-13-14
    Average 92 stars, based on 1 article reviews
    p p66shc - by Bioz Stars, 2026-09
    92/100 stars
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    p66Shc silencing was induced via lentiviruses delivered to C57BL/6 mice exposed to APAP (300 mg/kg). a , b Liver p66Shc, p52Shc, and p46Shc protein, n = 3. ** p < 0.01 vs. the control group. c Serum ALT levels, n = 8. d Serum AST levels, n = 8. e H&E staining. Scale bar, 200 μm. f , g Mitochondrial dynamics perturbation was determined via TEM (×2000/×10,000, magnification, red arrow). h Liver H 2 O 2 levels, n = 8. i Liver GSH levels, n = 8. j Liver MDA levels, n = 8. k , l Liver p66Shc, p-p66Shc, OMA1, L-OPA1, S-OPA1, MFN2, DRP1, p-DRP1 protein, n = 3. m , n Liver OMA1 ubiquitination level, n = 3. * p < 0.05, ** p < 0.01 vs. the LV-control group; # p < 0.05, ## p < 0.01 vs. the APAP group.

    Journal: Cell Death & Disease

    Article Title: circ-CBFB upregulates p66Shc to perturb mitochondrial dynamics in APAP-induced liver injury

    doi: 10.1038/s41419-020-03160-y

    Figure Lengend Snippet: p66Shc silencing was induced via lentiviruses delivered to C57BL/6 mice exposed to APAP (300 mg/kg). a , b Liver p66Shc, p52Shc, and p46Shc protein, n = 3. ** p < 0.01 vs. the control group. c Serum ALT levels, n = 8. d Serum AST levels, n = 8. e H&E staining. Scale bar, 200 μm. f , g Mitochondrial dynamics perturbation was determined via TEM (×2000/×10,000, magnification, red arrow). h Liver H 2 O 2 levels, n = 8. i Liver GSH levels, n = 8. j Liver MDA levels, n = 8. k , l Liver p66Shc, p-p66Shc, OMA1, L-OPA1, S-OPA1, MFN2, DRP1, p-DRP1 protein, n = 3. m , n Liver OMA1 ubiquitination level, n = 3. * p < 0.05, ** p < 0.01 vs. the LV-control group; # p < 0.05, ## p < 0.01 vs. the APAP group.

    Article Snippet: The primary antibodies included antibodies against the following: p66Shc (BD Biosciences, USA, 610878), p-p66Shc (Bioss, China, bs-3410R), CYP2E1 (Proteintech, China, 19937-1-AP), OMA1 (Santa, USA, sc-515788), OPA1 (Proteintech, China, 27733-1-AP), MFN2 (Bioss, China, bs-23685R), DRP1 (Wanleibio, China, WL03028), p-DRP1 (Abcam, USA, ab193216), and beta-actin (Proteintech, China, 60008-1-Ig).

    Techniques: Staining

    a AML12 cells were exposed to APAP (5 mM) and the p66Shc, p52Shc, and p46Shc proteins, n = 3. b – f AML12 cells were transfected with si-control or si-p66Shc and then exposed to APAP (5 mM). b H 2 O 2 levels, n = 8. c , d p66Shc, p-p66Shc, CYP2E1, OMA1, L-OPA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. e , f OMA1 ubiquitination level, n = 3. g , h AML12 cells were transfected with pcDNA 3.1 or pcDNA-p66Shc and then exposed to APAP and the p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. Mitochondrial ROS, cell apoptosis, and mitochondrial fragmentation were determined via representative fluorescence images of MitoSOX- ( i ), Tunel-( j ), and TOM20-stained ( k ) cells. Scale bar, 200 μm, 100 μm, or 12.5 μm. The colocalization of p66Shc and mitochondria (Mitotracker) ( l ), OMA1 and mitochondria (Mitotracker) ( m ) and p66Shc and OMA1 ( n ). Scale bar, 12.5 μm. ( o ) AML12 cells were transfected with si-control or si-p66Shc and then treated with APAP and MG132. Mitochondrial fragmentation was determined via representative fluorescence images of TOM20-stained cells. Scale bar, 12.5 μm. ** p < 0.01 vs. the si-control group; ## p < 0.01 vs. the APAP group; && p < 0.01 vs. the si-p66Shc group.

    Journal: Cell Death & Disease

    Article Title: circ-CBFB upregulates p66Shc to perturb mitochondrial dynamics in APAP-induced liver injury

    doi: 10.1038/s41419-020-03160-y

    Figure Lengend Snippet: a AML12 cells were exposed to APAP (5 mM) and the p66Shc, p52Shc, and p46Shc proteins, n = 3. b – f AML12 cells were transfected with si-control or si-p66Shc and then exposed to APAP (5 mM). b H 2 O 2 levels, n = 8. c , d p66Shc, p-p66Shc, CYP2E1, OMA1, L-OPA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. e , f OMA1 ubiquitination level, n = 3. g , h AML12 cells were transfected with pcDNA 3.1 or pcDNA-p66Shc and then exposed to APAP and the p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. Mitochondrial ROS, cell apoptosis, and mitochondrial fragmentation were determined via representative fluorescence images of MitoSOX- ( i ), Tunel-( j ), and TOM20-stained ( k ) cells. Scale bar, 200 μm, 100 μm, or 12.5 μm. The colocalization of p66Shc and mitochondria (Mitotracker) ( l ), OMA1 and mitochondria (Mitotracker) ( m ) and p66Shc and OMA1 ( n ). Scale bar, 12.5 μm. ( o ) AML12 cells were transfected with si-control or si-p66Shc and then treated with APAP and MG132. Mitochondrial fragmentation was determined via representative fluorescence images of TOM20-stained cells. Scale bar, 12.5 μm. ** p < 0.01 vs. the si-control group; ## p < 0.01 vs. the APAP group; && p < 0.01 vs. the si-p66Shc group.

    Article Snippet: The primary antibodies included antibodies against the following: p66Shc (BD Biosciences, USA, 610878), p-p66Shc (Bioss, China, bs-3410R), CYP2E1 (Proteintech, China, 19937-1-AP), OMA1 (Santa, USA, sc-515788), OPA1 (Proteintech, China, 27733-1-AP), MFN2 (Bioss, China, bs-23685R), DRP1 (Wanleibio, China, WL03028), p-DRP1 (Abcam, USA, ab193216), and beta-actin (Proteintech, China, 60008-1-Ig).

    Techniques: Transfection, Fluorescence, TUNEL Assay, Staining

    AML12 cells were transected with pcDNA 3.1 or pcDNA-p66Shc and then incubated with mito-TEMPO under APAP treatment. a Mitochondrial ROS were determined via representative fluorescence images of MitoSOX-stained cells. Scale bar, 200 μm. b , c OMA1, S-OPA1, MFN2, DRP1, p-DRP1 protein, n = 3. d OMA1 ubiquitination level, n = 3. ** p < 0.01 vs. the pcDNA 3.1 group; ## p < 0.01 vs. the APAP group; && p < 0.01 vs. the pcDNA-p66Shc group.

    Journal: Cell Death & Disease

    Article Title: circ-CBFB upregulates p66Shc to perturb mitochondrial dynamics in APAP-induced liver injury

    doi: 10.1038/s41419-020-03160-y

    Figure Lengend Snippet: AML12 cells were transected with pcDNA 3.1 or pcDNA-p66Shc and then incubated with mito-TEMPO under APAP treatment. a Mitochondrial ROS were determined via representative fluorescence images of MitoSOX-stained cells. Scale bar, 200 μm. b , c OMA1, S-OPA1, MFN2, DRP1, p-DRP1 protein, n = 3. d OMA1 ubiquitination level, n = 3. ** p < 0.01 vs. the pcDNA 3.1 group; ## p < 0.01 vs. the APAP group; && p < 0.01 vs. the pcDNA-p66Shc group.

    Article Snippet: The primary antibodies included antibodies against the following: p66Shc (BD Biosciences, USA, 610878), p-p66Shc (Bioss, China, bs-3410R), CYP2E1 (Proteintech, China, 19937-1-AP), OMA1 (Santa, USA, sc-515788), OPA1 (Proteintech, China, 27733-1-AP), MFN2 (Bioss, China, bs-23685R), DRP1 (Wanleibio, China, WL03028), p-DRP1 (Abcam, USA, ab193216), and beta-actin (Proteintech, China, 60008-1-Ig).

    Techniques: Incubation, Fluorescence, Staining

    a miR-185-5p has a predicted binding site in p66Shc from humans and mice. b Liver miR-185-5p expression, n = 6. c Hepatocytes miR-185-5p expression, n = 6. * p < 0.05, ** p < 0.01 vs. the control group. d , e AML12 cells were transfected with agomir-NC or miR-185-5p agomir. d miR-185-5p expression, n = 6. e p66Shc protein, n = 3. ** p < 0.01 vs. the ago-NC group. f , g AML12 cells were transfected with antagomir-NC or miR-185-5p antagomir. f miR-185-5p expression, n = 6. g p66Shc protein, n = 3. ** p < 0.01 vs. the ant-NC group. h AML12 cells were transfected with wild-type or mutant SHC1-3′-UTR luciferase constructs and with agomir-NC or miR-185-5p agomir. Luciferase activity was detected 48 h after transfection. ** p < 0.01 vs. the ago-NC group.

    Journal: Cell Death & Disease

    Article Title: circ-CBFB upregulates p66Shc to perturb mitochondrial dynamics in APAP-induced liver injury

    doi: 10.1038/s41419-020-03160-y

    Figure Lengend Snippet: a miR-185-5p has a predicted binding site in p66Shc from humans and mice. b Liver miR-185-5p expression, n = 6. c Hepatocytes miR-185-5p expression, n = 6. * p < 0.05, ** p < 0.01 vs. the control group. d , e AML12 cells were transfected with agomir-NC or miR-185-5p agomir. d miR-185-5p expression, n = 6. e p66Shc protein, n = 3. ** p < 0.01 vs. the ago-NC group. f , g AML12 cells were transfected with antagomir-NC or miR-185-5p antagomir. f miR-185-5p expression, n = 6. g p66Shc protein, n = 3. ** p < 0.01 vs. the ant-NC group. h AML12 cells were transfected with wild-type or mutant SHC1-3′-UTR luciferase constructs and with agomir-NC or miR-185-5p agomir. Luciferase activity was detected 48 h after transfection. ** p < 0.01 vs. the ago-NC group.

    Article Snippet: The primary antibodies included antibodies against the following: p66Shc (BD Biosciences, USA, 610878), p-p66Shc (Bioss, China, bs-3410R), CYP2E1 (Proteintech, China, 19937-1-AP), OMA1 (Santa, USA, sc-515788), OPA1 (Proteintech, China, 27733-1-AP), MFN2 (Bioss, China, bs-23685R), DRP1 (Wanleibio, China, WL03028), p-DRP1 (Abcam, USA, ab193216), and beta-actin (Proteintech, China, 60008-1-Ig).

    Techniques: Binding Assay, Expressing, Transfection, Mutagenesis, Luciferase, Construct, Activity Assay

    AML12 cells were transfected with agomir-NC or miR-185-5p agomir and then exposed to APAP. a , b p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. c Mitochondrial fragmentation was determined via representative fluorescence images of TOM20-stained cells. Scale bar, 12.5 μm. * p < 0.05, ** p < 0.01 vs. the ago-NC group; # p < 0.05, ## p < 0.01 vs. the APAP group.

    Journal: Cell Death & Disease

    Article Title: circ-CBFB upregulates p66Shc to perturb mitochondrial dynamics in APAP-induced liver injury

    doi: 10.1038/s41419-020-03160-y

    Figure Lengend Snippet: AML12 cells were transfected with agomir-NC or miR-185-5p agomir and then exposed to APAP. a , b p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. c Mitochondrial fragmentation was determined via representative fluorescence images of TOM20-stained cells. Scale bar, 12.5 μm. * p < 0.05, ** p < 0.01 vs. the ago-NC group; # p < 0.05, ## p < 0.01 vs. the APAP group.

    Article Snippet: The primary antibodies included antibodies against the following: p66Shc (BD Biosciences, USA, 610878), p-p66Shc (Bioss, China, bs-3410R), CYP2E1 (Proteintech, China, 19937-1-AP), OMA1 (Santa, USA, sc-515788), OPA1 (Proteintech, China, 27733-1-AP), MFN2 (Bioss, China, bs-23685R), DRP1 (Wanleibio, China, WL03028), p-DRP1 (Abcam, USA, ab193216), and beta-actin (Proteintech, China, 60008-1-Ig).

    Techniques: Transfection, Fluorescence, Staining

    AML12 cells were transfected with si-control or si-CBFB and ant-NC or miR-185-5p antagomir and then exposed to APAP. a circ-CBFB expression, n = 6. b , c p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. d Mitochondrial fragmentation was determined via representative fluorescence images of TOM20-stained cells. Scale bar, 12.5 μm. e , f p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. g Mitochondrial fragmentation was determined via representative fluorescence images of TOM20-stained cells. Scale bar, 12.5 μm. ** p < 0.01 vs. the si-control group; ## p < 0.01 vs. the APAP group; && p < 0.01 vs. the si-CBFB group.

    Journal: Cell Death & Disease

    Article Title: circ-CBFB upregulates p66Shc to perturb mitochondrial dynamics in APAP-induced liver injury

    doi: 10.1038/s41419-020-03160-y

    Figure Lengend Snippet: AML12 cells were transfected with si-control or si-CBFB and ant-NC or miR-185-5p antagomir and then exposed to APAP. a circ-CBFB expression, n = 6. b , c p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. d Mitochondrial fragmentation was determined via representative fluorescence images of TOM20-stained cells. Scale bar, 12.5 μm. e , f p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. g Mitochondrial fragmentation was determined via representative fluorescence images of TOM20-stained cells. Scale bar, 12.5 μm. ** p < 0.01 vs. the si-control group; ## p < 0.01 vs. the APAP group; && p < 0.01 vs. the si-CBFB group.

    Article Snippet: The primary antibodies included antibodies against the following: p66Shc (BD Biosciences, USA, 610878), p-p66Shc (Bioss, China, bs-3410R), CYP2E1 (Proteintech, China, 19937-1-AP), OMA1 (Santa, USA, sc-515788), OPA1 (Proteintech, China, 27733-1-AP), MFN2 (Bioss, China, bs-23685R), DRP1 (Wanleibio, China, WL03028), p-DRP1 (Abcam, USA, ab193216), and beta-actin (Proteintech, China, 60008-1-Ig).

    Techniques: Transfection, Expressing, Fluorescence, Staining

    circ-CBFB and miR-185-5p silencing was induced via lentiviruses delivered to C57BL/6 mice exposed to APAP. a H&E staining. Scale bar, 200 μm. b , c Mitochondrial dynamics perturbation was determined via TEM (×2000/×10,000, magnification, red arrow). d Serum ALT levels, n = 8. e Serum AST levels, n = 8. f Liver GSH levels, n = 8. g Liver MDA levels, n = 8. h , i Liver p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. ** p < 0.01 vs. the LV-control group; ## p < 0.01 vs. the APAP group; & p < 0.05, && p < 0.01 vs. the LV-CBFB group.

    Journal: Cell Death & Disease

    Article Title: circ-CBFB upregulates p66Shc to perturb mitochondrial dynamics in APAP-induced liver injury

    doi: 10.1038/s41419-020-03160-y

    Figure Lengend Snippet: circ-CBFB and miR-185-5p silencing was induced via lentiviruses delivered to C57BL/6 mice exposed to APAP. a H&E staining. Scale bar, 200 μm. b , c Mitochondrial dynamics perturbation was determined via TEM (×2000/×10,000, magnification, red arrow). d Serum ALT levels, n = 8. e Serum AST levels, n = 8. f Liver GSH levels, n = 8. g Liver MDA levels, n = 8. h , i Liver p66Shc, OMA1, S-OPA1, MFN2, DRP1, and p-DRP1 proteins, n = 3. ** p < 0.01 vs. the LV-control group; ## p < 0.01 vs. the APAP group; & p < 0.05, && p < 0.01 vs. the LV-CBFB group.

    Article Snippet: The primary antibodies included antibodies against the following: p66Shc (BD Biosciences, USA, 610878), p-p66Shc (Bioss, China, bs-3410R), CYP2E1 (Proteintech, China, 19937-1-AP), OMA1 (Santa, USA, sc-515788), OPA1 (Proteintech, China, 27733-1-AP), MFN2 (Bioss, China, bs-23685R), DRP1 (Wanleibio, China, WL03028), p-DRP1 (Abcam, USA, ab193216), and beta-actin (Proteintech, China, 60008-1-Ig).

    Techniques: Staining