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primary antibody against ir β  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc primary antibody against ir β
    Primary Antibody Against Ir β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 527 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+against+insulin+receptor+(insr/Insulin+Receptor+beta+Rabbit+mAb/pmc11914097-19-0-5
    Average 96 stars, based on 527 article reviews
    primary antibody against ir β - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    other:

    Article Title: Sea cucumber derived sulfated sterols alter glucose metabolism by promoting gluconeogenesis and reducing glycogenesis in healthy mice
    Article Snippet: All primary antibodies against insulin receptor (InsR) (#bs-0681R), p-InsR (#bs-16680R), protein kinase B (AKT) (#9272), p-AKT (#4060), glycogen synthase kinase-3 beta (GSK3β) (#bs-0023M), p-GSK3β (#bs-5367R), forkhead box protein O1 (FOXO1) (#9454), p-FOXO1 (#9461), GLUT4 (#bs-0384R), Na, K-ATPase (#3010), β-actin (#4967) and secondary antibodies were obtained from Cell Signaling Technology (Beverly, USA) and BIOSS (Beijing, China).

    Article Title: Loss of Slc12a2 specifically in pancreatic β-cells drives metabolic syndrome in mice
    Article Snippet: The primary antibodies used were directed against: insulin receptor β-subunit (Insr) , the S/T protein kinase Akt and its active version p Akt phosphorylated in S 473 (rabbit, Cell Signaling #3025, #9272 and #9271, respectively), the catalytic subunit of glucose-6-phosphatase G6Pc (rabbit, Abcam ab83690) and β-actin (mouse, Developmental Studies Hybridoma Bank #528068).

    Article Title: Sea cucumber derived sulfated sterols alter glucose metabolism by promoting gluconeogenesis and reducing glycogenesis in healthy mice
    Article Snippet: Blots were blocked in 5% bovine serum albumin (BSA) and then incubated with primary antibodies against InsR (1:1 000, BIOSS), p-InsR (1:1 000, BIOSS), AKT (1:1 000, Cell Signaling Technology), p-AKT (1:1 000, Cell Signaling Technology), GSK3β (1:1 000, BIOSS), p-GSK3β (1:1 000, BIOSS), FOXO1 (1:2 000, Cell Signaling Technology), p-FOXO1 (1:2 000, Cell Signaling Technology), GLUT4 (1:1 000, BIOSS), Na, K-ATPase (1:1 000, Cell Signaling Technology), at 4 °C overnight respectively.

    Article Title: Loss of Slc12a2 specifically in pancreatic β-cells drives metabolic syndrome in mice.
    Article Snippet: The primary antibodies used were directed against: insulin receptor β-subunit (Insr), the S/T protein kinase Akt and its active version pAkt phosphorylated in S473 (rabbit, Cell Signaling #3025, #9272 and #9271, respectively), the catalytic subunit of glucose-6-phosphatase G6Pc (rabbit, Abcam ab83690) and β-actin (mouse, Developmental Studies Hybridoma Bank #528068).

    Article Title: A decrease in Flavonifractor plautii and its product, phytosphingosine, predisposes individuals with phlegm-dampness constitution to metabolic disorders
    Article Snippet: Primary antibody against p-IR-β , Cell Signaling Technology, Inc., Shanghai, China , #2381.

    Membrane:

    Article Title: The IGF-1R Inhibitor NVP-AEW541 Causes Insulin-Independent and Reversible Cardiac Contractile Dysfunction
    Article Snippet: .. 40 μg) was loaded to a 10% polyacrylamide gel and separated at 40 mA for 1 h. After SDS-PAGE, the proteins were transferred to a PDVF membrane and incubated with primary antibodies against InsR/IGF-1R (Tyr999) (#3025, Cell Signaling), Phospho-InsR/IGF-1R (Tyr 1135/1136 and Tyr1150/1151) (#3024S, Cell Signaling), Akt (binding to peptide corresponding to the carboxy-terminal sequence) (#9272S, Cell Signaling), Phospho-Akt (Ser473) (#9271S, Cell Signaling), and secondary antibody (#NA934V, AbChem). ..

    Article Title: The IGF-1R Inhibitor NVP-AEW541 Causes Insulin-Independent and Reversible Cardiac Contractile Dysfunction.
    Article Snippet: .. 40 μg) was loaded to a 10% polyacrylamide gel and separated at 40 mA for 1 h. After SDS-PAGE, the proteins were transferred to a PDVF membrane and incubated with primary antibodies against InsR/IGF-1R (Tyr999) (#3025, Cell Signaling), Phospho-InsR/IGF-1R (Tyr 1135/1136 and Tyr1150/1151) (#3024S, Cell Signaling), Akt (binding to peptide corresponding to the carboxy-terminal sequence) (#9272S, Cell Signaling), Phospho-Akt (Ser473) (#9271S, Cell Signaling), and secondary antibody (#NA934V, AbChem). ..

    Incubation:

    Article Title: The IGF-1R Inhibitor NVP-AEW541 Causes Insulin-Independent and Reversible Cardiac Contractile Dysfunction
    Article Snippet: .. 40 μg) was loaded to a 10% polyacrylamide gel and separated at 40 mA for 1 h. After SDS-PAGE, the proteins were transferred to a PDVF membrane and incubated with primary antibodies against InsR/IGF-1R (Tyr999) (#3025, Cell Signaling), Phospho-InsR/IGF-1R (Tyr 1135/1136 and Tyr1150/1151) (#3024S, Cell Signaling), Akt (binding to peptide corresponding to the carboxy-terminal sequence) (#9272S, Cell Signaling), Phospho-Akt (Ser473) (#9271S, Cell Signaling), and secondary antibody (#NA934V, AbChem). ..

    Article Title: The IGF-1R Inhibitor NVP-AEW541 Causes Insulin-Independent and Reversible Cardiac Contractile Dysfunction.
    Article Snippet: .. 40 μg) was loaded to a 10% polyacrylamide gel and separated at 40 mA for 1 h. After SDS-PAGE, the proteins were transferred to a PDVF membrane and incubated with primary antibodies against InsR/IGF-1R (Tyr999) (#3025, Cell Signaling), Phospho-InsR/IGF-1R (Tyr 1135/1136 and Tyr1150/1151) (#3024S, Cell Signaling), Akt (binding to peptide corresponding to the carboxy-terminal sequence) (#9272S, Cell Signaling), Phospho-Akt (Ser473) (#9271S, Cell Signaling), and secondary antibody (#NA934V, AbChem). ..

    Binding Assay:

    Article Title: The IGF-1R Inhibitor NVP-AEW541 Causes Insulin-Independent and Reversible Cardiac Contractile Dysfunction
    Article Snippet: .. 40 μg) was loaded to a 10% polyacrylamide gel and separated at 40 mA for 1 h. After SDS-PAGE, the proteins were transferred to a PDVF membrane and incubated with primary antibodies against InsR/IGF-1R (Tyr999) (#3025, Cell Signaling), Phospho-InsR/IGF-1R (Tyr 1135/1136 and Tyr1150/1151) (#3024S, Cell Signaling), Akt (binding to peptide corresponding to the carboxy-terminal sequence) (#9272S, Cell Signaling), Phospho-Akt (Ser473) (#9271S, Cell Signaling), and secondary antibody (#NA934V, AbChem). ..

    Article Title: The IGF-1R Inhibitor NVP-AEW541 Causes Insulin-Independent and Reversible Cardiac Contractile Dysfunction.
    Article Snippet: .. 40 μg) was loaded to a 10% polyacrylamide gel and separated at 40 mA for 1 h. After SDS-PAGE, the proteins were transferred to a PDVF membrane and incubated with primary antibodies against InsR/IGF-1R (Tyr999) (#3025, Cell Signaling), Phospho-InsR/IGF-1R (Tyr 1135/1136 and Tyr1150/1151) (#3024S, Cell Signaling), Akt (binding to peptide corresponding to the carboxy-terminal sequence) (#9272S, Cell Signaling), Phospho-Akt (Ser473) (#9271S, Cell Signaling), and secondary antibody (#NA934V, AbChem). ..

    Sequencing:

    Article Title: The IGF-1R Inhibitor NVP-AEW541 Causes Insulin-Independent and Reversible Cardiac Contractile Dysfunction
    Article Snippet: .. 40 μg) was loaded to a 10% polyacrylamide gel and separated at 40 mA for 1 h. After SDS-PAGE, the proteins were transferred to a PDVF membrane and incubated with primary antibodies against InsR/IGF-1R (Tyr999) (#3025, Cell Signaling), Phospho-InsR/IGF-1R (Tyr 1135/1136 and Tyr1150/1151) (#3024S, Cell Signaling), Akt (binding to peptide corresponding to the carboxy-terminal sequence) (#9272S, Cell Signaling), Phospho-Akt (Ser473) (#9271S, Cell Signaling), and secondary antibody (#NA934V, AbChem). ..

    Article Title: The IGF-1R Inhibitor NVP-AEW541 Causes Insulin-Independent and Reversible Cardiac Contractile Dysfunction.
    Article Snippet: .. 40 μg) was loaded to a 10% polyacrylamide gel and separated at 40 mA for 1 h. After SDS-PAGE, the proteins were transferred to a PDVF membrane and incubated with primary antibodies against InsR/IGF-1R (Tyr999) (#3025, Cell Signaling), Phospho-InsR/IGF-1R (Tyr 1135/1136 and Tyr1150/1151) (#3024S, Cell Signaling), Akt (binding to peptide corresponding to the carboxy-terminal sequence) (#9272S, Cell Signaling), Phospho-Akt (Ser473) (#9271S, Cell Signaling), and secondary antibody (#NA934V, AbChem). ..



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    Cell Signaling Technology Inc primary antibody against ir β
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    Image Search Results


    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)

    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

    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

    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

    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

    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

    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

    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

    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.

    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