sirt2 polyclonal antibody  (Proteintech)

Journal: iScience

Article Title: Mitochondrial glycerol 3-phosphate dehydrogenase deficiency exacerbates lipotoxic cardiomyopathy

doi: 10.1016/j.isci.2024.109796

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Article Snippet: Rabbit polyclonal anti-SIRT2 antibody , Proteintech , Cat# 19655-1-AP; RRID: AB_2878592.

Techniques: Virus, Recombinant, Modification, Transfection, Labeling, XF Assay, Isolation, Staining, Bicinchoninic Acid Protein Assay, Immunoprecipitation, Plasmid Preparation, Control, Software

Journal: eLife

Article Title: SIRT2 inhibition protects against cardiac hypertrophy and ischemic injury

doi: 10.7554/eLife.85571

Figure Lengend Snippet: ( A ) SIRT1, SIRT2, SIRT3, and SIRT6 in mouse hearts after trans-aortic constriction (TAC). ( B ) SIRT2 in human hearts from healthy patients and patients with dilated cardiomyopathy. ( C ) SIRT2 protein levels in the hearts of control individual and patients with ischemic heart failure. *p<0.05 by Student’s t-test. Data presented as mean ± SEM. Figure 1—source data 1. SIRT1, -2, -3, and -6 after sham and trans-aortic constriction (TAC) surgery as shown in . Figure 1—source data 2. SIRT2 in non-failing and failing human hearts as shown in . Figure 1—source data 3. SIRT2 in non-failing and ischemic human hearts as shown in . Figure 1—source data 4. Full gels for . Figure 1—source data 5. Full gels for unedited. Figure 1—source data 6. Full gels for unedited.

Article Snippet: Antibody , Rabbit polyclonal SIRT2 antibody , Sigma , S8447 , WB (1:1000).

Techniques:

Journal: eLife

Article Title: SIRT2 inhibition protects against cardiac hypertrophy and ischemic injury

doi: 10.7554/eLife.85571

Figure Lengend Snippet: Sirt2 -/- and wild-type (WT) littermates were subjected to TAC and ejection fraction (EF) ( A ), fractional shortening (FS) ( B ), and interventricular septal thickness during diastole ( C ) were assessed 4 weeks later (N=6–9). ( D–F ) Representative hearts ( D ), HW/BW ( E ) (N=3–5), H&E staining, ( F ) and the summary of cross-sectional area of cardiomyocytes ( G ) in WT and Sirt2 -/- hearts (N=20 cardiomyocytes), *p<0.05 by one-way ANOVA and post hoc Tukey analysis ( A, B, C, and E ) and unpaired Student’s t-test ( G ). Bars represent group mean. Figure 2—source data 1. Ejection fraction (EF) in wild-type (WT) and Sirt2 -/- mice after sham or trans-aortic constriction (TAC) as shown in . Figure 2—source data 2. Fractional shortening (FS) in wild-type (WT) and Sirt2 -/- mice after sham or trans-aortic constriction (TAC) as shown in . Figure 2—source data 3. Interventricular septal (IVS) thickness diastole in wild-type (WT) and Sirt2 -/- mice after sham or trans-aortic constriction (TAC) as shown in . Figure 2—source data 4. HW/BW in wild-type (WT) and Sirt2 -/- mice after sham or trans-aortic constriction (TAC) as shown in . Figure 2—source data 5. CSA in wild-type (WT) and Sirt2 -/- hearts as shown in .

Article Snippet: Antibody , Rabbit polyclonal SIRT2 antibody , Sigma , S8447 , WB (1:1000).

Techniques: Staining

Journal: eLife

Article Title: SIRT2 inhibition protects against cardiac hypertrophy and ischemic injury

doi: 10.7554/eLife.85571

Figure Lengend Snippet: Ejection fraction (EF) and fractional shortening (FS) in Sirt2 f/f and cs- Sirt2 -/- mice 7 ( A ) and 14 days ( B ) after TAC (N=5–9). ( C,D ) mRNA levels of Anf ( C ) and Bnp ( D ) in the hearts of Sirt2 f/f and cs- Sirt2 -/- mice 4 weeks after TAC (N=7–8). ( E ) EF and FS in Sirt2 f/f and cs- Sirt2 -/- mice 7 and 14 days after I/R (N=4). ( F ) Necrotic area (representing the degree of ischemic damage) in Sirt2 f/f and cs- Sirt2 -/- mice 14 days after MI. *p<0.05 by ANOVA for panels A and B, and Student’s t-test was used for panels C and D. Data are presented as mean ± SEM. Figure 4—source data 1. Ejection fraction (EF) and fractional shortening (FS) in Sirt2 f/f and cs- Sirt2 -/- mice 7 days after ischemia-reperfusion (I/R) as shown in . Figure 4—source data 2. Ejection fraction (EF) and fractional shortening (FS) in Sirt2 f/f and cs- Sirt2 -/- mice 14 days after ischemia-reperfusion (I/R) as shown in . Figure 4—source data 3. Nppa mRNA in Sirt2 f/f and cs- Sirt2 -/- hearts as shown in . Figure 4—source data 4. Nppb mRNA in Sirt2 f/f and cs- Sirt2 -/- hearts as shown in . Figure 4—source data 5. Echo parameters in Sirt2 f/f and cs- Sirt2 -/- hearts as shown in .

Article Snippet: Antibody , Rabbit polyclonal SIRT2 antibody , Sigma , S8447 , WB (1:1000).

Techniques:

Journal: eLife

Article Title: SIRT2 inhibition protects against cardiac hypertrophy and ischemic injury

doi: 10.7554/eLife.85571

Figure Lengend Snippet: ( A ) Co-immunoprecipitation (IP) of SIRT2 and NRF2 in extracts of hearts from wild-type (WT) mice. ( B ) Endogenous NRF2 acetylation levels in the hearts of WT and Sirt2 -/- mice at the baseline. Acetylated proteins were IPed by anti-acetyl antibody followed by immunoblotting with anti-NRF2 antibody. ( C ) NRF2 protein levels in neonatal rat cardiomyocytes (NRCMs) treated with Sirt2 siRNA. ( D ) NRF2 protein levels in H9c2 cells treated with control or Sirt2 siRNA and harvested at different time points after treatment with 100 µg/ml of CHX. ( E ) NRF2 protein levels in the nucleus in NRCMs treated with control or Sirt2 siRNA. ( F–H ) mRNA levels of NRF2 target genes in pentose phosphate pathway ( F ), quinone and glutathione-based detoxification ( G ), thioredoxin production ( H ) in H9c2 cells overexpressing empty vector (white bars) or SIRT2 (gray bars). *p<0.05 by Student’s t-test. Figure 5—source data 1. mRNA with overexpression of EV or SIRT2 as shown in . Figure 5—source data 2. mRNA with overexpression of EV or SIRT2 as shown in . Figure 5—source data 3. mRNA with overexpression of EV or SIRT2 as shown in . Figure 5—source data 4. Uncropped gels for . Figure 5—source data 5. Uncropped gels for unedited. Figure 5—source data 6. Uncropped gels for unedited.

Article Snippet: Antibody , Rabbit polyclonal SIRT2 antibody , Sigma , S8447 , WB (1:1000).

Techniques: Immunoprecipitation, Western Blot, Plasmid Preparation, Over Expression

Journal: eLife

Article Title: SIRT2 inhibition protects against cardiac hypertrophy and ischemic injury

doi: 10.7554/eLife.85571

Figure Lengend Snippet:

Article Snippet: Antibody , Rabbit polyclonal SIRT2 antibody , Sigma , S8447 , WB (1:1000).

Techniques: Knock-Out, Activity Assay, In Vivo, Protease Inhibitor, Transfection, SYBR Green Assay, Bicinchoninic Acid Protein Assay, Extraction, Staining, Sequencing, Recombinant, Plasmid Preparation, Software

Journal: Journal of Neuroimmune Pharmacology

Article Title: SIRT2 Inhibition Rescues Neurodegenerative Pathology but Increases Systemic Inflammation in a Transgenic Mouse Model of Alzheimer’s Disease

doi: 10.1007/s11481-023-10084-9

Figure Lengend Snippet: SIRT2 inhibition increases microglial phagocytosis of methoxy-labeled Aβ. ( a ) Experimental design for quantitative in vivo assessment of amyloid-beta phagocytic capacity and gating strategy to identify CD11b + CD45 low microglia. SSC: side scatter; FSC: forward scatter. ( b ) Quantification of Aβ phagocytosis by flow cytometry of microglia isolated from vehicle or 33i treated 8 months-old APP/PS1 mice 3 h after intraperitoneal injection of methoxy-X04 (*p < 0.05, Student’s t-test). Results are shown as mean ± SEM (n = 5–6 animals per group). ( c ) Representative FACS plots demonstrating the engulfment of Aβ by microglia isolated from APP/PS1 mice upon treatment with vehicle or 33i. Wild-type mice (WT) injected with methoxy-X04 were used to determine the methoxy-X04-threshold for non-phagocytic cells

Article Snippet: The trans-blots were blocked in TBS-Tween containing 5% powder milk for 1 h. Membranes were probed overnight at 4 °C with rabbit polyclonal antibody anti-SIRT2 (1:1000; cat# S8447, Sigma-Aldrich).

Techniques: Inhibition, Labeling, In Vivo, Flow Cytometry, Isolation, Injection

Journal: Journal of Neuroimmune Pharmacology

Article Title: SIRT2 Inhibition Rescues Neurodegenerative Pathology but Increases Systemic Inflammation in a Transgenic Mouse Model of Alzheimer’s Disease

doi: 10.1007/s11481-023-10084-9

Figure Lengend Snippet: SIRT2 inhibition induces peripheral inflammation. ( a ) Weekly body weight monitoring of WT and APP/PS1 mice during the treatment. Glucose ( b ) and Insulin ( c ) tolerance tests. 33i treatment for two months in WT and APP/PS1 mice did not have any significant effect on glucose and insulin tolerance (n = 12–14 animals per group). ( d ) Gene expression of Il-1β (F = 7.529, *p < 0.05, main effect of treatment; F = 5.532, #p < 0.05, main effect of genotype, two-way ANOVA, n = 5–6 mice per group) and ( e ) protein expression of IL-1β (F = 50.13, ***p < 0.01, main effect of treatment; F = 4.978, #p < 0.05, main effect of genotype, two-way ANOVA, n = 7–8 animals per group) in white adipose tissue of WT and APP/PS1 mice. Note that 33i treatment increased levels of this pro-inflammatory cytokine in WT and APP/PS1 animals. Peripheral gene expression of ( f ) Tnf-α (F = 5.201, *p < 0.05, main effect of treatment; F = 21.11, ###p < 0.001, main effect of genotype, two-way ANOVA) and ( g ) Tgf-β (F = 11.46, ##p < 0.01, main effect of genotype, two-way ANOVA) (n = 5–6 animals per group). 36b4 was used as an internal control. Serum levels of the cytokines ( h ) IL-6 (F = 18.76, ***p < 0.001, main effect of treatment, two-way ANOVA), ( i ) MCP-1 (F = 7.782, *p < 0.05, main effect of treatment, two-way ANOVA) and ( j ) TNF (F = 8.901, **p < 0.01, main effect of treatment, two-way ANOVA) (n = 5–8 mice per group). Results are shown as mean ± SEM

Article Snippet: The trans-blots were blocked in TBS-Tween containing 5% powder milk for 1 h. Membranes were probed overnight at 4 °C with rabbit polyclonal antibody anti-SIRT2 (1:1000; cat# S8447, Sigma-Aldrich).

Techniques: Inhibition, Expressing

Journal: Journal of Neuroimmune Pharmacology

Article Title: SIRT2 Inhibition Rescues Neurodegenerative Pathology but Increases Systemic Inflammation in a Transgenic Mouse Model of Alzheimer’s Disease

doi: 10.1007/s11481-023-10084-9

Figure Lengend Snippet: Peripheral SIRT2 inhibition impairs memory and increases systemic inflammation. ( a ) Habituation phase of the MWM. ( b ) Escape latency in the acquisition phase of the MWM and corresponding area under the curve (AUC) of the acquisition curve (F = 6.716, *p < 0.05 main effect of treatment; F = 6.580, #p < 0.05 main effect of genotype, two-way ANOVA, n = 6–8 animals per group). Note that AGK-2 treatment worsened learning capacities in both WT and APP/PS1 mice. ( c ) Representation of the percentage of time spent in the correct quadrant in the retention phase of the MWM (5 th Day: F = 4.474 *p < 0.05, main effect of treatment; 8 th Day: F = 4.854, #p < 0.05, main effect of genotype, two-way ANOVA). ( d ) Representative hippocampal sections of β-amyloid plaques stained with 6E10 antibody in brain slices (left) and amyloid burden quantification (right) in 8 months-old APP/PS1 mice treated for two months with vehicle or AGK-2 (n = 3 animals per group, 2 sections including hippocampus and frontal cortex per animal) Scale bar = 500 µm. Glucose ( e ) and Insulin ( f ) tolerance tests. No significant differences were observed between vehicle or AGK-2 treated animals (n = 5–9 mice per group). Peripheral protein expression of ( g ) IL-1β (F = 5.951, *p < 0.05, main effect of treatment, two-way ANOVA) and gene expression of ( h ) Il-1β (F = 16.33, ***p < 0.001, main effect of treatment, two-way ANOVA), ( i ) Tnf-α (F = 19.60, ***p < 0.001, main effect of treatment, two-way ANOVA) and ( j ) Tgf-β (F = 11.49, **p < 0.01, main effect of treatment, two-way ANOVA) (n = 6 animals per group). 36b4 was used as an internal control. Serum levels of the cytokines ( k ) IL-6 (F = 10.80, ***p < 0.001, main effect of treatment, two-way ANOVA), ( l ) MCP-1 and ( m ) TNF (F = 5.926, *p < 0.05, main effect of treatment, two-way ANOVA) (n = 5–8 mice per group). Results are shown as mean ± SEM

Article Snippet: The trans-blots were blocked in TBS-Tween containing 5% powder milk for 1 h. Membranes were probed overnight at 4 °C with rabbit polyclonal antibody anti-SIRT2 (1:1000; cat# S8447, Sigma-Aldrich).

Techniques: Inhibition, Staining, Expressing

Journal: Journal of Neuroimmune Pharmacology

Article Title: SIRT2 Inhibition Rescues Neurodegenerative Pathology but Increases Systemic Inflammation in a Transgenic Mouse Model of Alzheimer’s Disease

doi: 10.1007/s11481-023-10084-9

Figure Lengend Snippet: SIRT2 is increased in postmortem brain tissue from Alzheimer’s disease patients but not in serum. ( a ) Gene expression of SIRT2 in frontal cortex of postmortem control and Alzheimer’s disease (AD) human samples (*p < 0.05, Student’s t-test). β-ACTIN was used as internal control (n = 10 samples per group). ( b ) Representative western blot images (top) and SIRT2 protein levels quantification (bottom) in frontal cortex of postmortem control and AD human samples (*p < 0.05, Student’s t-test). β-ACTIN was used as internal control (n = 7 samples per group). ( c ) No significant differences between both groups were found when SIRT2 was analysed in serum samples (n = 24 samples per group)

Article Snippet: The trans-blots were blocked in TBS-Tween containing 5% powder milk for 1 h. Membranes were probed overnight at 4 °C with rabbit polyclonal antibody anti-SIRT2 (1:1000; cat# S8447, Sigma-Aldrich).

Techniques: Expressing, Western Blot