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Cell Signaling Technology Inc pirs1
Pirs1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pirs1/pm41036740-42-20-14
Average 86 stars, based on 1 article reviews

pirs1 - by Bioz Stars, 2026-10

86/100 stars

Images

Phospho-proteomics:

Article Title: Cytokeratin 8 as a Novel Therapeutic Target in Type 2 Diabetes Mellitus: Suppression of Hepatic Glycogen Synthesis via IRS1/PI3K/Akt/GSK3β Signaling.
Article Snippet: Department of Endocrinology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, 710004, P.R.. China; National & Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, 710004, P.R.. China; Department of General Surgery, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, 710004, P.R.

Blocking Assay:

Article Title: B1344 ameliorates non-alcoholic steatohepatitis in HFCD-HF/G-induced mice: exploring the therapeutic efficacy and mechanism of a novel FGF21 analogue.
Article Snippet: The endocrine cytokine, fibroblast growth factor 21 (FGF21), shows therapeutic potential for non-alcoholic steatohepatitis (NASH) but has pharmacokinetic limitations.. B1344 is a modified PEGylated FGF21 analogue with enhanced stability and bioactivity.. Researches are required to further explore its effect and possible mechanisms against NASH.

Membrane:

Incubation:

Article Title: Influence of Exercise and Genistein to Mitigate the Deleterious Effects of High-Fat High-Sugar Diet on Alzheimer’s Disease-Related Markers in Male Mice
Article Snippet: .. Blots were loaded with 5 ug protein/lane and individually incubated with each of the following primary antibodies overnight at 4 °C: pGSk-3ß (1:1000, Cell Signaling #5558, Danvers, MA, USA), GSK-3ß (1:1000, Cell Signaling #9315, Danvers, MA, USA), Caspase-3 (1:1000, Cell Signaling #9662, Danvers, MA, USA), 4G8 (1:500, BioLegend #SIG-39200, San Diego, CA, USA), CP13 (1:1000, Cell Signaling #39357, Danvers, MA, USA), 22c11 (1:1000, Millipore #MAB348, St. Louis, MO, USA), CT20 (1:1000, Millipore #171610, St. Louis, MO, USA), ADAM10 (1:1000, Cell Signaling #14194, Danvers, MA, USA), p-IR (1:1000, Cell Signaling #3026, Danvers, MA, USA), IR (1:500, Santa Cruz #sc-373975, Dallas, TX, USA), pIRS1 (1:1000, Cell Signaling #2386, Danvers, MA, USA), IRS1 (1:1000, Millipore-Sigma #06-248, Burlington, MA, USA), GLUT1 (1:500, Alomone #AGT-021, Jerusalem, Israel). .. Blots were either re-probed for actin (anti-actin primary antibody, 1:4000, Thermo Scientific, Rockford, IL, USA) or re-probed for GAPDH (anti-GAPDH primary antibody, 1:4000, Thermo Scientific, Rockford, IL, USA) for 1 h at room temperature to serve as the control.

Imaging:

Cell-Signaling:

Lysis:

Article Title: Brain insulin signaling and cerebrovascular disease in human postmortem brain
Article Snippet: .. After thawing, tissue was homogenized in lysis buffer and supernatant aliquots were assayed in duplicate using the PathScan ® ELISA kit, a solid phase sandwich ELISA (Cell Signaling, Danvers, MA): measurements obtained were on the total IRS1, catalog #7328; pIRS1 (S307), catalog #7287; AKT1, catalog #7170; and pAKT1 (Thr308), catalog #7252. ..

Enzyme-linked Immunosorbent Assay:

Sandwich ELISA:

other:

Article Title: Short-Term Diet Induced Changes in the Central and Circulating IGF Systems Are Sex Specific
Article Snippet: pIRS1 (Ser 789) , Polyclonal , 1:750 , Rabbit , Cell Signaling , 2389 .

Image Search Results

a Insulin signaling activity in primary hepatocytes from ERα F/F and ERα LivKO male mice, n = 3 independent cells; for IRS1, ERα F/F -Vehicle versus ERα LivKO -Vehicle, P < 0.0001, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001; for pAKT-S473, ERα F/F -Vehicle versus ERα F/F -Insulin, P < 0.0001, ERα LivKO -Vehicle versus ERα LivKO -Insulin, P = 0.0186, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001; for ERα , ERα F/F -Vehicle versus ERα LivKO -Vehicle, P = 0.0002, ERα F/F -Insulin versus ERα LivKO -Insulin, P = 0.0001. b Effect of ERα gain-of-function on hepatic insulin sensitivity. The experiments were repeated independently twice. Representative blots were shown. c Effect of ERα deletion on insulin-induced IRS1 and p85 interaction. The experiments were repeated independently twice. Representative blots were shown. d Effect of ERα gain-of-function on insulin-induced IRS1 and p85 interaction. The experiments were repeated independently twice. Representative blots were shown. e Effect of ERα deletion on mRNA expression of Irs1 and Irs2 in primary mouse hepatocytes, n = 4 ( ERα F/F ) and 5 ( ERα LivKO ); for ERα , P = 0.0001. f Interaction between ERα and IRS1 or IRS2 in HEK293T cells. The experiments were repeated independently three times. Representative blots were shown. g Effect of ERα on IRS1 ubiquitination in HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. h Effect of ERα on IRS2 ubiquitination in HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. i Effect of ERα deletion on IRS1 ubiquitinat i on in primary mouse hepatocytes. The experiments were repeated independently twice. Representative blots were shown. j Diagram of IRS1 and its truncated domains. k Interaction between ERα and IRS1 domains in HEK293T cells. The experiments were repeated independently three times. Representative blots were shown. l Effect of ERα deletion on IRS1 phosphorylation in primary mouse hepatocytes, n = 3 independent cells; for IRS1, P = 0.0102; for pIRS1-S302, P = 0.0236. m Effect of ERα gain-of-function on palmitate-induced insulin resistance in primary mouse hepatocytes. The experiments were repeated independently twice. Representative blots were shown. Data are presented as mean ± SEM. * P < 0.05 , *** P < 0.001, **** P < 0.0001, unpaired Two-tailed Student’s t test (e and l), Two-way ANOVA with Tukey’s multiple comparisons test (a). Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: An estrogen receptor α-derived peptide improves glucose homeostasis during obesity

doi: 10.1038/s41467-024-47687-6

Figure Lengend Snippet: a Insulin signaling activity in primary hepatocytes from ERα F/F and ERα LivKO male mice, n = 3 independent cells; for IRS1, ERα F/F -Vehicle versus ERα LivKO -Vehicle, P < 0.0001, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001; for pAKT-S473, ERα F/F -Vehicle versus ERα F/F -Insulin, P < 0.0001, ERα LivKO -Vehicle versus ERα LivKO -Insulin, P = 0.0186, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001; for ERα , ERα F/F -Vehicle versus ERα LivKO -Vehicle, P = 0.0002, ERα F/F -Insulin versus ERα LivKO -Insulin, P = 0.0001. b Effect of ERα gain-of-function on hepatic insulin sensitivity. The experiments were repeated independently twice. Representative blots were shown. c Effect of ERα deletion on insulin-induced IRS1 and p85 interaction. The experiments were repeated independently twice. Representative blots were shown. d Effect of ERα gain-of-function on insulin-induced IRS1 and p85 interaction. The experiments were repeated independently twice. Representative blots were shown. e Effect of ERα deletion on mRNA expression of Irs1 and Irs2 in primary mouse hepatocytes, n = 4 ( ERα F/F ) and 5 ( ERα LivKO ); for ERα , P = 0.0001. f Interaction between ERα and IRS1 or IRS2 in HEK293T cells. The experiments were repeated independently three times. Representative blots were shown. g Effect of ERα on IRS1 ubiquitination in HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. h Effect of ERα on IRS2 ubiquitination in HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. i Effect of ERα deletion on IRS1 ubiquitinat i on in primary mouse hepatocytes. The experiments were repeated independently twice. Representative blots were shown. j Diagram of IRS1 and its truncated domains. k Interaction between ERα and IRS1 domains in HEK293T cells. The experiments were repeated independently three times. Representative blots were shown. l Effect of ERα deletion on IRS1 phosphorylation in primary mouse hepatocytes, n = 3 independent cells; for IRS1, P = 0.0102; for pIRS1-S302, P = 0.0236. m Effect of ERα gain-of-function on palmitate-induced insulin resistance in primary mouse hepatocytes. The experiments were repeated independently twice. Representative blots were shown. Data are presented as mean ± SEM. * P < 0.05 , *** P < 0.001, **** P < 0.0001, unpaired Two-tailed Student’s t test (e and l), Two-way ANOVA with Tukey’s multiple comparisons test (a). Source data are provided as a Source Data file.

Article Snippet: The membrane was then incubated with primary antibodies including anti-IRS1 antibody (Cell Signaling Technology, Cat# 2390, Dilution: 1:1000), anti-IRS2 antibody (Cell Signaling Technology, Cat# 4502, Dilution: 1:1000), anti-pAKT-S473 antibody (Cell Signaling Technology, Cat# 9271, Dilution: 1:1000), anti-pAKT-T308 antibody (Cell Signaling Technology, Cat# 13038, Dilution: 1:1000), anti-AKT antibody (Cell Signaling Technology, Cat# 4691, Dilution: 1:1000), anti-ERα antibody (Cell Signaling Technology, Cat# 13258, Dilution: 1:1000), anti-pIRS1-S302 antibody (Cell Signaling Technology, Cat# 2384, Dilution: 1:1000), anti-pIRS1-S307 antibody (Cell Signaling Technology, Cat# 2381, Dilution: 1:1000), anti-pIRS1-S636/639 antibody (Cell Signaling Technology, Cat# 2388, Dilution: 1:1000), anti-pIRS1-S1101 antibody (Cell Signaling Technology, Cat# 2385, Dilution: 1:1000), anti-p85 antibody (Cell Signaling Technology, Cat# 4292, Dilution: 1:1000), anti-Ubiquitin antibody (Cell Signaling Technology, Cat# 58395, Dilution: 1:1000), anti-HA antibody (Cell Signaling Technology, Cat# 2367, Dilution: 1:1000), anti-Flag antibody (Cell Signaling Technology, Cat# 8146, Dilution: 1:1000), and anti-GAPDH antibody (Cell Signaling Technology, Cat# 5174, Dilution: 1:3000) at 4 °C overnight, followed by secondary antibody incubation (anti-rabbit IgG HRP-linked, Cell Signaling Technology, Cat# 7074, Dilution: 1:3000 and anti-mouse IgG HRP-linked, Cell Signaling Technology, Cat# 7076, Dilution: 1:3000) for 1 h at room temperature.

Techniques: Activity Assay, Expressing, Ubiquitin Proteomics, Phospho-proteomics, Two Tailed Test

a Diagram of truncated ERα protein domains. b Effect of ERα on insulin sensitivity in HepG2 cells, n = 3 independent cells; for IRS1, Vehicle versus ERα-Vehicle, P < 0.0001, Insulin versus ERα-Insulin, P = 0.0005; for pAKT-S473, Vehicle versus ERα-Vehicle, P = 0.0025, Vehicle versus Insulin, P < 0.0001, ERα-Vehicle versus ERα-Insulin, P < 0.0001, Insulin versus ERα-Insulin, P = 0.0001; for pAKT-T308, Vehicle versus Insulin, P < 0.0001, ERα-Vehicle versus ERα-Insulin, P < 0.0001, Insulin versus ERα-Insulin, P < 0.0001. c Effect of ERα 1-280 on insulin sensitivity in HepG2 cells, n = 3 independent cells; for IRS1, Vehicle versus ERα 1-280-Vehicle, P < 0.0001, Insulin versus ERα 1-280-Insulin, P = 0.0034; for pAKT-S473, Vehicle versus ERα 1-280-Vehicle, P = 0.0457, Vehicle versus Insulin, P < 0.0001, ERα 1-280-Vehicle versus ERα 1-280-Insulin, P < 0.0001, Insulin versus ERα 1-280-Insulin, P = 0.0007; for pAKT-T308, Vehicle versus Insulin, P = 0.0040, ERα 1-280-Vehicle versus ERα 1-280-Insulin, P = 0.0003, Insulin versus ERα 1-280-Insulin, P = 0.0397. d Effect of ERα DBD + AF2 on insulin sensitivity in HepG2 cells, n = 3 independent cells; for pAKT-S473, Vehicle versus Insulin, P < 0.0001, ERα DBD + AF2-Vehicle versus ERα DBD + AF2-Insulin, P < 0.0001; for pAKT-T308, Vehicle versus Insulin, P = 0.0002, ERα DBD + AF2-Vehicle versus ERα DBD + AF2-Insulin, P = 0.0003. e Interaction between ERα 1-280 and IRS1 protein domains. The experiments were repeated independently twice. Representativ e blots were shown. f Effect of ERα 1-280 on IRS1 phosphorylation at S302 in HepG2 cells, n = 3 independent cells; for pIRS1-S302, P = 0.0227; for IRS1, P = 0.0187. g Effect of ERα on IRS1 phosphorylation at S302 in HepG2 cells, n = 3 independent cells; for pIRS1-S302, P = 0.0207; for IRS1, P = 0.0154. h Effect of ERα 1-280 on IRS1 ubiquitination i n HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. i Effect of ERα 1-280 on IRS2 ubiquitination in HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, unpaired Two-tailed Student’s t test ( f , g ), Two-way ANOVA with Tukey’s multiple comparisons test ( b , c , d ). CNTR: Control. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: An estrogen receptor α-derived peptide improves glucose homeostasis during obesity

doi: 10.1038/s41467-024-47687-6

Figure Lengend Snippet: a Diagram of truncated ERα protein domains. b Effect of ERα on insulin sensitivity in HepG2 cells, n = 3 independent cells; for IRS1, Vehicle versus ERα-Vehicle, P < 0.0001, Insulin versus ERα-Insulin, P = 0.0005; for pAKT-S473, Vehicle versus ERα-Vehicle, P = 0.0025, Vehicle versus Insulin, P < 0.0001, ERα-Vehicle versus ERα-Insulin, P < 0.0001, Insulin versus ERα-Insulin, P = 0.0001; for pAKT-T308, Vehicle versus Insulin, P < 0.0001, ERα-Vehicle versus ERα-Insulin, P < 0.0001, Insulin versus ERα-Insulin, P < 0.0001. c Effect of ERα 1-280 on insulin sensitivity in HepG2 cells, n = 3 independent cells; for IRS1, Vehicle versus ERα 1-280-Vehicle, P < 0.0001, Insulin versus ERα 1-280-Insulin, P = 0.0034; for pAKT-S473, Vehicle versus ERα 1-280-Vehicle, P = 0.0457, Vehicle versus Insulin, P < 0.0001, ERα 1-280-Vehicle versus ERα 1-280-Insulin, P < 0.0001, Insulin versus ERα 1-280-Insulin, P = 0.0007; for pAKT-T308, Vehicle versus Insulin, P = 0.0040, ERα 1-280-Vehicle versus ERα 1-280-Insulin, P = 0.0003, Insulin versus ERα 1-280-Insulin, P = 0.0397. d Effect of ERα DBD + AF2 on insulin sensitivity in HepG2 cells, n = 3 independent cells; for pAKT-S473, Vehicle versus Insulin, P < 0.0001, ERα DBD + AF2-Vehicle versus ERα DBD + AF2-Insulin, P < 0.0001; for pAKT-T308, Vehicle versus Insulin, P = 0.0002, ERα DBD + AF2-Vehicle versus ERα DBD + AF2-Insulin, P = 0.0003. e Interaction between ERα 1-280 and IRS1 protein domains. The experiments were repeated independently twice. Representativ e blots were shown. f Effect of ERα 1-280 on IRS1 phosphorylation at S302 in HepG2 cells, n = 3 independent cells; for pIRS1-S302, P = 0.0227; for IRS1, P = 0.0187. g Effect of ERα on IRS1 phosphorylation at S302 in HepG2 cells, n = 3 independent cells; for pIRS1-S302, P = 0.0207; for IRS1, P = 0.0154. h Effect of ERα 1-280 on IRS1 ubiquitination i n HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. i Effect of ERα 1-280 on IRS2 ubiquitination in HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, unpaired Two-tailed Student’s t test ( f , g ), Two-way ANOVA with Tukey’s multiple comparisons test ( b , c , d ). CNTR: Control. Source data are provided as a Source Data file.

Techniques: Phospho-proteomics, Ubiquitin Proteomics, Two Tailed Test, Control

a SVM score of interaction between IRS1 and ERα domains. b Effect of ERα 1-60 domain and AF1 peptide (34 aa) on insulin sensitivity in HepG2 cells, n = 3 independent cells; for IRS1, Insulin versus 34 aa peptide-Insulin, P = 0.0046, Insulin versus ERα 1-60-Insulin, P = 0.0006; for pAKT-S473, Vehicle versus Insulin, P < 0.0001, Insulin versus 34 aa peptide-Insulin, P = 0.0044, Insulin versus ERα 1-60-Insulin, P = 0.0030. c Effect of ERα 60-280 domain on insulin sensitivity in HepG2 cells, n = 3 indepe n dent cells; for pAKT-S473, Vehicle versus Insulin, P < 0.0001, ERα 60-280-Vehicle versus ERα 60-280-Insulin, P < 0.0001. d Immunofluorescence staining of AF1 peptide (34 aa) and ERα 1-60 domain in HEK293T cells. The experiments were repeated independently twice. Representative images were shown. e Amino acid sequence of FITC labeled AF1 peptide conjugated with TAT. f Interaction between AF1 peptide and IRS1 protein domains. The experiments were repeated independently twice. Representative results were shown. g Effect of AF1 peptide on IRS1 phosphorylation at S302 in primary mouse hepatocytes, n = 3 independent cells; for pIRS1-S302, P = 0.0377; for IRS1, P = 0.0156. h Effect of AF1 peptide on IRS1 ubiquitination in HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. i Effect of AF1 peptide on insulin-induced suppression of HGP in primary hepatocytes upon glucagon treatment, n = 4 independent cells; CNTR-Vehicle versus CNTR-Glucagon, P = 0.0006, AF1 peptide-Vehicle versus AF1 peptide-Glucagon, P = 0.0272, CNTR-Glucagon-Insulin versus AF1 peptide-Glucagon-Insulin, P = 0.0019. j Effect of AF1 peptide on insulin sensitivity in primary mouse hepatocytes, n = 3 independent cells; for IRS1, CNTR-Vehicle versus AF1 peptide-Vehicle, P = 0.0067, CNTR-Insulin versus AF1 peptide-Insulin, P = 0.0314, for pAKT-S473, AF1 peptide-Vehicle versus AF1 peptide-Insulin, P = 0.0001, CNTR-Insulin versus AF1 peptide-Insulin, P = 0.0008; for pAKT-T308, CNTR-Vehicle versus CNTR-Insulin, P = 0.0154, AF1 peptide-Vehicle versus AF1 peptide-Insulin, P = 0.0002, CNTR-Insulin versus AF1 peptide-Insulin, P = 0.0167. k Effect of AF1 peptide on insulin sensitivity in control and ERα deficient primary mouse hepatocytes, n = 3 independent cells, for IRS1, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001, ERα LivKO -Insulin versus ERα LivKO -Insuin-AF1 peptide, P = 0.0061, for pAKT-S473, ERα F/F -Vehicle versus ERα F/F -Insulin, P < 0.0001, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001, ERα LivKO -Insulin versus ERα LivKO -Insulin-AF1 peptide, P = 0.0034; for pAKT-T308, ERα F/F -Vehicle versus ERα F/F -Insulin, P < 0.0001, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001, ERα LivKO -Insulin versus ERα LivKO -Insulin-AF1 peptide, P = 0.0090. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, unpaired Two-tailed Student’s t test ( g ), One-way ANOVA ( b , i , k ), Two-way ANOVA with Tukey’s multiple comparisons test ( c , j ). CNTR: Control. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: An estrogen receptor α-derived peptide improves glucose homeostasis during obesity

doi: 10.1038/s41467-024-47687-6

Figure Lengend Snippet: a SVM score of interaction between IRS1 and ERα domains. b Effect of ERα 1-60 domain and AF1 peptide (34 aa) on insulin sensitivity in HepG2 cells, n = 3 independent cells; for IRS1, Insulin versus 34 aa peptide-Insulin, P = 0.0046, Insulin versus ERα 1-60-Insulin, P = 0.0006; for pAKT-S473, Vehicle versus Insulin, P < 0.0001, Insulin versus 34 aa peptide-Insulin, P = 0.0044, Insulin versus ERα 1-60-Insulin, P = 0.0030. c Effect of ERα 60-280 domain on insulin sensitivity in HepG2 cells, n = 3 indepe n dent cells; for pAKT-S473, Vehicle versus Insulin, P < 0.0001, ERα 60-280-Vehicle versus ERα 60-280-Insulin, P < 0.0001. d Immunofluorescence staining of AF1 peptide (34 aa) and ERα 1-60 domain in HEK293T cells. The experiments were repeated independently twice. Representative images were shown. e Amino acid sequence of FITC labeled AF1 peptide conjugated with TAT. f Interaction between AF1 peptide and IRS1 protein domains. The experiments were repeated independently twice. Representative results were shown. g Effect of AF1 peptide on IRS1 phosphorylation at S302 in primary mouse hepatocytes, n = 3 independent cells; for pIRS1-S302, P = 0.0377; for IRS1, P = 0.0156. h Effect of AF1 peptide on IRS1 ubiquitination in HEK293T cells. The experiments were repeated independently twice. Representative blots were shown. i Effect of AF1 peptide on insulin-induced suppression of HGP in primary hepatocytes upon glucagon treatment, n = 4 independent cells; CNTR-Vehicle versus CNTR-Glucagon, P = 0.0006, AF1 peptide-Vehicle versus AF1 peptide-Glucagon, P = 0.0272, CNTR-Glucagon-Insulin versus AF1 peptide-Glucagon-Insulin, P = 0.0019. j Effect of AF1 peptide on insulin sensitivity in primary mouse hepatocytes, n = 3 independent cells; for IRS1, CNTR-Vehicle versus AF1 peptide-Vehicle, P = 0.0067, CNTR-Insulin versus AF1 peptide-Insulin, P = 0.0314, for pAKT-S473, AF1 peptide-Vehicle versus AF1 peptide-Insulin, P = 0.0001, CNTR-Insulin versus AF1 peptide-Insulin, P = 0.0008; for pAKT-T308, CNTR-Vehicle versus CNTR-Insulin, P = 0.0154, AF1 peptide-Vehicle versus AF1 peptide-Insulin, P = 0.0002, CNTR-Insulin versus AF1 peptide-Insulin, P = 0.0167. k Effect of AF1 peptide on insulin sensitivity in control and ERα deficient primary mouse hepatocytes, n = 3 independent cells, for IRS1, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001, ERα LivKO -Insulin versus ERα LivKO -Insuin-AF1 peptide, P = 0.0061, for pAKT-S473, ERα F/F -Vehicle versus ERα F/F -Insulin, P < 0.0001, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001, ERα LivKO -Insulin versus ERα LivKO -Insulin-AF1 peptide, P = 0.0034; for pAKT-T308, ERα F/F -Vehicle versus ERα F/F -Insulin, P < 0.0001, ERα F/F -Insulin versus ERα LivKO -Insulin, P < 0.0001, ERα LivKO -Insulin versus ERα LivKO -Insulin-AF1 peptide, P = 0.0090. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, unpaired Two-tailed Student’s t test ( g ), One-way ANOVA ( b , i , k ), Two-way ANOVA with Tukey’s multiple comparisons test ( c , j ). CNTR: Control. Source data are provided as a Source Data file.

Techniques: Immunofluorescence, Staining, Sequencing, Labeling, Phospho-proteomics, Ubiquitin Proteomics, Control, Two Tailed Test

a Body weight of db/db mice treated with control and AF1 peptide for 5 weeks, n = 5 (AF1 peptide) and 6 (control) mice/group. b Random feeding and 16 h fasting blood glucose in db/db mice treated with control and AF1 peptide for 5 weeks, n = 6 mice/group; fasting blood glucose, P = 0.0409; feeding blood glucose, P = 0.0317. c Glucose tolerance tests in db/db mice treated with control and AF1 peptide for 5 weeks, n = 6 mice/group; 0 min, P = 0.0409; 15 min, P = 0.0006; 30 min, P = 0.0032; 90 min, P = 0.0375; 120 min, P = 0.0104; AUC, P = 0.0042. d Insulin tolerance tests in db/db mice treated with control and AF1 peptide for 5 weeks, n = 6 mice/group; 30 min, P = 0.0328; 45 min, P = 0.0198, AUC, P = 0.0217. e H&E staining of livers from db/db mice treated with control and AF1 peptide. Scale: 200 µm. Liver fat content was calculated, n = 5 mice/group; P = 0.0013. Representative images were shown. f Liver insulin sensitivity in db/db mice treated with control and AF1 peptide, n = 5 mice/group; pIRS1-S302, P < 0.0001, IRS1, P = 0.0040, pAKT-S473, P = 0.0026, pAKT-T308, P = 0.0037. g Phosphorylation of AKT in epididymal fat and skeleton muscle from db/db mice treated with control and AF1 peptide, n = 4 mice/group; for fat, pAKT-S473, P = 0.0257, pAKT-T308, P = 0.0491, for muscle, pAKT-S473, P = 0.0069, pAKT-T308, P = 0.0450. h Volcano plots of differentially expressed genes (DEGs) in livers from db/db mice treated with control and AF1 peptide. Genes upregulated or downregulated by more than 1.3-fold are shown in red and blue, respectively. i KEGG pathway analysis of DEGs in livers from db/db mice treated with control and AF1 peptide. j Heatmap of representative DEGs in livers from db/db mice treated with control and AF1 peptide. k Liver triglyceride, serum triglyceride, AST, cholesterol, LDL, and NEFA levels in db/db mice treated with control and AF1 peptide, n = 4 (serum LDL of CNTR group), 5 (liver triglyceride and serum cholesterol of CNTR group as well as serum LDL and NEFA of AF1 peptide group), and 6 (serum triglyceride and AST of CNTR and AF1 peptide group, liver triglyceride and serum cholesterol of AF1 peptide group, and serum NEFAof CNTR group); serum AST, P = 0.0487, serum cholesterol, P = 0.0234, serum LDL, P = 0.0037, serum NEFA, P = 0.0411. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, unpaired Two-tailed Student’s t test. CNTR: Control. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: An estrogen receptor α-derived peptide improves glucose homeostasis during obesity

doi: 10.1038/s41467-024-47687-6

Figure Lengend Snippet: a Body weight of db/db mice treated with control and AF1 peptide for 5 weeks, n = 5 (AF1 peptide) and 6 (control) mice/group. b Random feeding and 16 h fasting blood glucose in db/db mice treated with control and AF1 peptide for 5 weeks, n = 6 mice/group; fasting blood glucose, P = 0.0409; feeding blood glucose, P = 0.0317. c Glucose tolerance tests in db/db mice treated with control and AF1 peptide for 5 weeks, n = 6 mice/group; 0 min, P = 0.0409; 15 min, P = 0.0006; 30 min, P = 0.0032; 90 min, P = 0.0375; 120 min, P = 0.0104; AUC, P = 0.0042. d Insulin tolerance tests in db/db mice treated with control and AF1 peptide for 5 weeks, n = 6 mice/group; 30 min, P = 0.0328; 45 min, P = 0.0198, AUC, P = 0.0217. e H&E staining of livers from db/db mice treated with control and AF1 peptide. Scale: 200 µm. Liver fat content was calculated, n = 5 mice/group; P = 0.0013. Representative images were shown. f Liver insulin sensitivity in db/db mice treated with control and AF1 peptide, n = 5 mice/group; pIRS1-S302, P < 0.0001, IRS1, P = 0.0040, pAKT-S473, P = 0.0026, pAKT-T308, P = 0.0037. g Phosphorylation of AKT in epididymal fat and skeleton muscle from db/db mice treated with control and AF1 peptide, n = 4 mice/group; for fat, pAKT-S473, P = 0.0257, pAKT-T308, P = 0.0491, for muscle, pAKT-S473, P = 0.0069, pAKT-T308, P = 0.0450. h Volcano plots of differentially expressed genes (DEGs) in livers from db/db mice treated with control and AF1 peptide. Genes upregulated or downregulated by more than 1.3-fold are shown in red and blue, respectively. i KEGG pathway analysis of DEGs in livers from db/db mice treated with control and AF1 peptide. j Heatmap of representative DEGs in livers from db/db mice treated with control and AF1 peptide. k Liver triglyceride, serum triglyceride, AST, cholesterol, LDL, and NEFA levels in db/db mice treated with control and AF1 peptide, n = 4 (serum LDL of CNTR group), 5 (liver triglyceride and serum cholesterol of CNTR group as well as serum LDL and NEFA of AF1 peptide group), and 6 (serum triglyceride and AST of CNTR and AF1 peptide group, liver triglyceride and serum cholesterol of AF1 peptide group, and serum NEFAof CNTR group); serum AST, P = 0.0487, serum cholesterol, P = 0.0234, serum LDL, P = 0.0037, serum NEFA, P = 0.0411. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, unpaired Two-tailed Student’s t test. CNTR: Control. Source data are provided as a Source Data file.

Techniques: Control, Staining, Phospho-proteomics, Two Tailed Test

Journal: Nature Communications

Article Title: An estrogen receptor α-derived peptide improves glucose homeostasis during obesity

doi: 10.1038/s41467-024-47687-6

Techniques: Activity Assay, Expressing, Ubiquitin Proteomics, Phospho-proteomics, Two Tailed Test

Journal: Nature Communications

Article Title: An estrogen receptor α-derived peptide improves glucose homeostasis during obesity

doi: 10.1038/s41467-024-47687-6

Techniques: Phospho-proteomics, Ubiquitin Proteomics, Two Tailed Test, Control

Journal: Nature Communications

Article Title: An estrogen receptor α-derived peptide improves glucose homeostasis during obesity

doi: 10.1038/s41467-024-47687-6

Techniques: Immunofluorescence, Staining, Sequencing, Labeling, Phospho-proteomics, Ubiquitin Proteomics, Control, Two Tailed Test

Journal: Nature Communications

Article Title: An estrogen receptor α-derived peptide improves glucose homeostasis during obesity

doi: 10.1038/s41467-024-47687-6

Techniques: Control, Staining, Phospho-proteomics, Two Tailed Test

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