primary antibodies against insr  (Proteintech)

Journal: Scientific Reports

Article Title: Deciphering the hepatoprotective mechanism of Sarcopyramis nepalensis wall against non-alcoholic fatty liver disease by network pharmacology and experimental validation

doi: 10.1038/s41598-025-29480-7

Figure Lengend Snippet: Effect of S. nepalensis on the levels of InsR/PI3K/Akt/HIF-1α pathway proteins in livers of NAFLD-affected mice (n = 3).

Article Snippet: Primary antibodies against InsR (20433-1-AP, Proteintech, China), p-PI3K (YP0224, Immunoway, USA), PI3K (60225-1-Ig, Proteintech, China), p-Akt (YP0006, Immunoway, USA), Akt (YT0185, Immunoway, USA), HIF-1α (BF8002, Affinity, Melbourne), and β-actin (66009-1-Ig, Proteintech, China) were used.

Techniques:

Journal: Cell Discovery

Article Title: A decrease in Flavonifractor plautii and its product, phytosphingosine, predisposes individuals with phlegm-dampness constitution to metabolic disorders

doi: 10.1038/s41421-025-00789-x

Figure Lengend Snippet: Key materials and software.

Article Snippet: Primary antibody against p-IR-β , Cell Signaling Technology, Inc., Shanghai, China , #2381.

Techniques: Software, Recombinant, Luciferase, Reporter Gene Assay, Plasmid Preparation, Control, Transfection, Enzyme-linked Immunosorbent Assay, Staining

Journal: Diabetology & Metabolic Syndrome

Article Title: Effect of C-reactive protein deficiency on insulin resistance reversal in rats with polycystic ovary syndrome through augmented leptin action

doi: 10.1186/s13098-023-01155-1

Figure Lengend Snippet: Deficiency of CRP decreases susceptibility to DHEA and HFD-induced insulin resistance. Four-week-old of placebo or dehydroepiandrosterone (DHEA)-treated female WT and CRP KO rats were fed a ND or HFD for 3 month. (a, e) Blood glucose levels during the glucose tolerance test (GTT). (b, f) Area under curve (AUC) during the GTT. (c, g) Blood glucose levels during the insulin tolerance test (ITT). (d, h) AUC during the ITT.( * P < 0.05, ** P < 0.01vs WT group; # P < 0.05, ## P < 0.01 DHEA-WT group) (i) Experimental procedure and EHC protocol. (j) Glucose infusion rate (GIR) time course. (k) Cumulative GIR (l). Hepatic glucose production (HGP). (m) Percentage of suppression of HGP. (n) Glucose disappearance rates (GRD). (o) RT-PCR assays of hepatic PEPCK mRNA (p) Immunoblotting assays of hepatic expression of PEPCK protein, phosphorylation of InsR and Akt and densitometric quantification ( * P < 0.05, ** P < 0.01vs ND-DHEA-WT group; # P < 0.05, ## P < 0.01 HFD-DHEA-WT group). Data are expressed as the mean ± SEM (n = 6 rats for each group)

Article Snippet: Following this, the membranes were probed with 1:1,000 diluted primary antibodies against the insulin receptor (InsR) / phospho-InsR, AKT kinase (AKT) / phospho- AKT (Cell Signaling Technology, Beverly, MA, USA), PEPCK (Santa Cruz Biotechnology, Dallas, TX, USA); and GAPDH (Abcam, Cambridgeshire, UK) at 4 °C.

Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Expressing, Phospho-proteomics

Journal: Diabetology & Metabolic Syndrome

Article Title: Effect of C-reactive protein deficiency on insulin resistance reversal in rats with polycystic ovary syndrome through augmented leptin action

doi: 10.1186/s13098-023-01155-1

Figure Lengend Snippet: CRP deficiency enhance the role of peripheral leptin on restoring insulin sensitivity in PCOS rats fed a ND or HFD. (a) Experimental procedure and EHC protocol. (b) GIR time course (c) Cumulative GIR. (d) Hepatic glucose production (HGP). (e) Percentage of suppression of HGP. (f) Glucose disappearance rates (GRD). (g) RT-PCR assays of hepatic PEPCK mRNA (h, i) Immunoblotting assays of hepatic expression of PEPCK protein, phosphorylation of InsR and Akt and densitometric quantification. Data are expressed as the mean ± SEM (n = 5–6 rats for each group). * P < 0.05, ** P < 0.01 vs. ND-DHEA-WT group; # P < 0.05, ## P < 0.01 HFD-DHEA-WT group

Article Snippet: Following this, the membranes were probed with 1:1,000 diluted primary antibodies against the insulin receptor (InsR) / phospho-InsR, AKT kinase (AKT) / phospho- AKT (Cell Signaling Technology, Beverly, MA, USA), PEPCK (Santa Cruz Biotechnology, Dallas, TX, USA); and GAPDH (Abcam, Cambridgeshire, UK) at 4 °C.

Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Expressing, Phospho-proteomics

Journal: Diabetology & Metabolic Syndrome

Article Title: Effect of C-reactive protein deficiency on insulin resistance reversal in rats with polycystic ovary syndrome through augmented leptin action

doi: 10.1186/s13098-023-01155-1

Figure Lengend Snippet: CRP deficiency enhance the role of central leptin on restoring insulin sensitivity in PCOS rats fed a ND or HFD. (a) Experimental procedure and EHC protocol. (b) GIR time course (c) Cumulative GIR. (d) Hepatic glucose production (HGP). (e) Percentage of suppression of HGP. (f) Glucose disappearance rates (GRD). (g) RT-PCR assays of hepatic PEPCK mRNA (h, i) Immunoblotting assays of hepatic expression of PEPCK protein, phosphorylation of InsR and Akt and densitometric quantification. Data are expressed as the mean ± SEM (n = 5–6 rats for each group). * P < 0.05, ** P < 0.01 vs. ND-DHEA-WT group; # P < 0.05, ## P < 0.01 HFD-DHEA-WT group

Article Snippet: Following this, the membranes were probed with 1:1,000 diluted primary antibodies against the insulin receptor (InsR) / phospho-InsR, AKT kinase (AKT) / phospho- AKT (Cell Signaling Technology, Beverly, MA, USA), PEPCK (Santa Cruz Biotechnology, Dallas, TX, USA); and GAPDH (Abcam, Cambridgeshire, UK) at 4 °C.

Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Expressing, Phospho-proteomics

Journal: Diabetology & Metabolic Syndrome

Article Title: Effect of C-reactive protein deficiency on insulin resistance reversal in rats with polycystic ovary syndrome through augmented leptin action

doi: 10.1186/s13098-023-01155-1

Figure Lengend Snippet: CRP deficiency enhance the role of central leptin on restoring insulin sensitivity during lipid infusion in PCOS rats fed a ND. (a) Experimental procedure and EHC protocol. (b) GIR time course (c) Cumulative GIR. (d) Hepatic glucose production (HGP). (e) Percentage of suppression of HGP. (f) Glucose disappearance rates (GRD). (g) RT-PCR assays of hepatic PEPCK mRNA (h, i) Immunoblotting assays of hepatic expression of PEPCK protein, phosphorylation of InsR and Akt and densitometric quantification. Data are expressed as the mean ± SEM (n = 5–6 rats for each group). * P < 0.05, ** P < 0.01 vs. ND-DHEA-WT group

Article Snippet: Following this, the membranes were probed with 1:1,000 diluted primary antibodies against the insulin receptor (InsR) / phospho-InsR, AKT kinase (AKT) / phospho- AKT (Cell Signaling Technology, Beverly, MA, USA), PEPCK (Santa Cruz Biotechnology, Dallas, TX, USA); and GAPDH (Abcam, Cambridgeshire, UK) at 4 °C.

Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Expressing, Phospho-proteomics

Journal: Oncotarget

Article Title: Compounds from the marine sponge Cribrochalina vasculum offer a way to target IGF-1R mediated signaling in tumor cells

doi: 10.18632/oncotarget.10361

Figure Lengend Snippet: A. Western blot analyses of InsR α and InsR β in untreated diploid fibroblasts WI-38, NSCLC U-1810, breast cancer MDA-MB-231 and ovarian carcinoma A2780 or SKOV-3. β-Tubulin was used to visualize equal loading. Resulting bands were scanned by densitometry and fold to DMSO-treated cells is given after correction for loading differences. B. NSCLC U-1810 were treated with IC 50 of compound 1 (1.5 μmol/L) or 2 (15.1 μmol/L) for 4, 8, 16 and 24 hours or with equal volume of DMSO for 24 hours and InsR α and InsR β expression were examined. β-Tubulin was used to visualize equal loading. Resulting bands were scanned by densitometry and fold to DMSO-treated cells is given after correction for loading differences. C. NSCLC U-1810 cells were exposed to IC 50 of compound 1 (1.5 μmol/L). Slides were stained with two different InsR β antibodies in PLA (red) and DAPI (blue) was applied to visualize cell nuclei. Scale bars, 50 μm.

Article Snippet: Two primary antibodies against InsR β from different species (Rabbit: InsR-β, Cell signaling; 3025 and Mouse: InsR β, Abcam; AB69508) were applied.

Techniques: Western Blot, Expressing, Staining