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primary antibodies against phospho igf1r β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc primary antibodies against phospho igf1r β
    FIGURE 4 IGF-1 production and <t>IGF1R</t> signaling pathway activation in TA muscle of WT and MLC/mIgf-1 mice treatment with low TUN dose (0.1 mg/kg of TUN for 15 days). (A) Expression of endogenous Igf-1 mRNA isoforms (i.e., Igf-1Ea and Igf-1Ec mRNAs) and total Igf-1 (i.e., endogenous and mIgf-1 transgene mRNAs) in the TA muscle of WT (n = 3) and MLC/mIgf-1 (n = 3) mice treated with TUN. (B) Representative immunoblotting and (C) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using an antibody directed against mature mouse IGF-1 sequence. Three bands at a molecular weight of ~22, ~17, and ~12 kDa were detected in TA muscle of MLC/ mIgf1 mice. Recombinant mouse IGF-1 mature protein was loaded as a positive control for mature IGF-1 (~7 kDa). (D) Representative immunoblotting and (E) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (C) or two-way ANOVA followed by Tukey's multiple comparison post hoc tests (A, E). *Significantly different compared to CTR; #Significantly different compared to WT mice; * and # p ≤ .05; ** p ≤ .01 *** and ### p ≤ .001.
    Primary Antibodies Against Phospho Igf1r β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 430 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+against+phospho+igf1r+%CE%B2/Phospho-IGF-I+Receptor+beta+(Tyr1135%2F1136)%2FInsulin+Receptor+beta+(Tyr1150%2F1151)+Rabbit+mAb/10__1096_slash_fj__202400213rr-71-0-10
    Average 96 stars, based on 430 article reviews
    primary antibodies against phospho igf1r β - by Bioz Stars, 2026-10
    96/100 stars

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    1) Product Images from "Impaired myoblast differentiation and muscle IGF‐1 receptor signaling pathway activation after N‐glycosylation inhibition"

    Article Title: Impaired myoblast differentiation and muscle IGF‐1 receptor signaling pathway activation after N‐glycosylation inhibition

    Journal: The FASEB Journal

    doi: 10.1096/fj.202400213rr

    FIGURE 4 IGF-1 production and IGF1R signaling pathway activation in TA muscle of WT and MLC/mIgf-1 mice treatment with low TUN dose (0.1 mg/kg of TUN for 15 days). (A) Expression of endogenous Igf-1 mRNA isoforms (i.e., Igf-1Ea and Igf-1Ec mRNAs) and total Igf-1 (i.e., endogenous and mIgf-1 transgene mRNAs) in the TA muscle of WT (n = 3) and MLC/mIgf-1 (n = 3) mice treated with TUN. (B) Representative immunoblotting and (C) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using an antibody directed against mature mouse IGF-1 sequence. Three bands at a molecular weight of ~22, ~17, and ~12 kDa were detected in TA muscle of MLC/ mIgf1 mice. Recombinant mouse IGF-1 mature protein was loaded as a positive control for mature IGF-1 (~7 kDa). (D) Representative immunoblotting and (E) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (C) or two-way ANOVA followed by Tukey's multiple comparison post hoc tests (A, E). *Significantly different compared to CTR; #Significantly different compared to WT mice; * and # p ≤ .05; ** p ≤ .01 *** and ### p ≤ .001.
    Figure Legend Snippet: FIGURE 4 IGF-1 production and IGF1R signaling pathway activation in TA muscle of WT and MLC/mIgf-1 mice treatment with low TUN dose (0.1 mg/kg of TUN for 15 days). (A) Expression of endogenous Igf-1 mRNA isoforms (i.e., Igf-1Ea and Igf-1Ec mRNAs) and total Igf-1 (i.e., endogenous and mIgf-1 transgene mRNAs) in the TA muscle of WT (n = 3) and MLC/mIgf-1 (n = 3) mice treated with TUN. (B) Representative immunoblotting and (C) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using an antibody directed against mature mouse IGF-1 sequence. Three bands at a molecular weight of ~22, ~17, and ~12 kDa were detected in TA muscle of MLC/ mIgf1 mice. Recombinant mouse IGF-1 mature protein was loaded as a positive control for mature IGF-1 (~7 kDa). (D) Representative immunoblotting and (E) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (C) or two-way ANOVA followed by Tukey's multiple comparison post hoc tests (A, E). *Significantly different compared to CTR; #Significantly different compared to WT mice; * and # p ≤ .05; ** p ≤ .01 *** and ### p ≤ .001.

    Techniques Used: Activation Assay, Expressing, Western Blot, Sequencing, Molecular Weight, Recombinant, Positive Control, Comparison

    FIGURE 5 Effect of TUN treatment on IGF1R production and IGF1R signaling pathway activation in C2C12. (A) IGF1R and IGF1R proreceptor production in C2C12 cells treated with 0.01 μg/mL of TUN and harvested at day 1. (B) Immunofluorescence analysis of C2C12 cells stained with ant-IGF1R and DAPI, the scale bar represents 200 μm. (C) Representative immunoblotting and (D) band densitometry analysis of IGF-1-induced IGF-1R signaling pathway activation in CTR- and TUN-treated C2C12 cells using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. The calculation of pIGF1R level was normalized against total lysed protein instead of total IGF1R to account for the marked reduction of total IGF1R after TUN treatment. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (A) or one-way ANOVA followed by Tukey's multiple comparison post hoc tests (D). *Significantly different compared to CTR, #Significantly different compared to IGF-1-treated cells; ** p ≤ .01, *** p ≤ .001; ## p ≤ .01, ### p ≤ .001.
    Figure Legend Snippet: FIGURE 5 Effect of TUN treatment on IGF1R production and IGF1R signaling pathway activation in C2C12. (A) IGF1R and IGF1R proreceptor production in C2C12 cells treated with 0.01 μg/mL of TUN and harvested at day 1. (B) Immunofluorescence analysis of C2C12 cells stained with ant-IGF1R and DAPI, the scale bar represents 200 μm. (C) Representative immunoblotting and (D) band densitometry analysis of IGF-1-induced IGF-1R signaling pathway activation in CTR- and TUN-treated C2C12 cells using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. The calculation of pIGF1R level was normalized against total lysed protein instead of total IGF1R to account for the marked reduction of total IGF1R after TUN treatment. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (A) or one-way ANOVA followed by Tukey's multiple comparison post hoc tests (D). *Significantly different compared to CTR, #Significantly different compared to IGF-1-treated cells; ** p ≤ .01, *** p ≤ .001; ## p ≤ .01, ### p ≤ .001.

    Techniques Used: Activation Assay, Immunofluorescence, Staining, Western Blot, Comparison

    Related Articles

    Incubation:

    Article Title: Impaired myoblast differentiation and muscle <scp>IGF</scp>‐1 receptor signaling pathway activation after N‐glycosylation inhibition
    Article Snippet: The protein samples (20–30 μg total proteins) were electrophoresed through 10% SDS- PAGE, and then transferred to nitrocellulose or PVDF membranes (Bio- Rad Laboratories) for immunoblotting. .. Primary antibodies against phospho- IGF1R β (1:2000; cat. n. 3024 Cell Signaling Technology), total IGF1R β (1:2000; cat. n. 3027 Cell Signaling Technology), phospho- Akt (Ser473) (1:2000; cat. n. 9271 Cell Signaling Technology), total Akt (1:2000; cat. n. 9272 Cell Signaling Technology), phospho- p44/42 (ERK1/2) (1:2000; cat. n. 9101 Cell Signaling Technology), total p44/42 (ERK1/2) (1:2000; cat. n. 9102 Cell Signaling Technology), PCNA (1:5000, cat. n. MAB 424R Millipore), MF20 (1:500, DSHB), and mouse/rat biotinylated IGF- 1 antibody (1:300, cat. n. BAF791 R&D Systems) were incubated overnight at 4°C. .. For lectin blotting, membranes were probed with biotinylated Concanavalin A (Con A, 1:1000), Phaseolus vulgaris leucoagglutinin (PHA- L, 1:200), and Aleuria Aurantia (AAL, 1:400) lectins (Vector laboratories, D.B.A.



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    primary antibodies against phospho igf1r β  (Cell Signaling Technology Inc)
    96
    Cell Signaling Technology Inc primary antibodies against phospho igf1r β
    FIGURE 4 IGF-1 production and <t>IGF1R</t> signaling pathway activation in TA muscle of WT and MLC/mIgf-1 mice treatment with low TUN dose (0.1 mg/kg of TUN for 15 days). (A) Expression of endogenous Igf-1 mRNA isoforms (i.e., Igf-1Ea and Igf-1Ec mRNAs) and total Igf-1 (i.e., endogenous and mIgf-1 transgene mRNAs) in the TA muscle of WT (n = 3) and MLC/mIgf-1 (n = 3) mice treated with TUN. (B) Representative immunoblotting and (C) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using an antibody directed against mature mouse IGF-1 sequence. Three bands at a molecular weight of ~22, ~17, and ~12 kDa were detected in TA muscle of MLC/ mIgf1 mice. Recombinant mouse IGF-1 mature protein was loaded as a positive control for mature IGF-1 (~7 kDa). (D) Representative immunoblotting and (E) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (C) or two-way ANOVA followed by Tukey's multiple comparison post hoc tests (A, E). *Significantly different compared to CTR; #Significantly different compared to WT mice; * and # p ≤ .05; ** p ≤ .01 *** and ### p ≤ .001.
    Primary Antibodies Against Phospho Igf1r β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+against+phospho+igf1r+%CE%B2/Phospho-IGF-I+Receptor+beta+(Tyr1135%2F1136)%2FInsulin+Receptor+beta+(Tyr1150%2F1151)+Rabbit+mAb/10__1096_slash_fj__202400213rr-71-0-10
    Average 96 stars, based on 1 article reviews
    primary antibodies against phospho igf1r β - by Bioz Stars, 2026-10
    96/100 stars
    		  Buy from Supplier

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    FIGURE 4 IGF-1 production and IGF1R signaling pathway activation in TA muscle of WT and MLC/mIgf-1 mice treatment with low TUN dose (0.1 mg/kg of TUN for 15 days). (A) Expression of endogenous Igf-1 mRNA isoforms (i.e., Igf-1Ea and Igf-1Ec mRNAs) and total Igf-1 (i.e., endogenous and mIgf-1 transgene mRNAs) in the TA muscle of WT (n = 3) and MLC/mIgf-1 (n = 3) mice treated with TUN. (B) Representative immunoblotting and (C) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using an antibody directed against mature mouse IGF-1 sequence. Three bands at a molecular weight of ~22, ~17, and ~12 kDa were detected in TA muscle of MLC/ mIgf1 mice. Recombinant mouse IGF-1 mature protein was loaded as a positive control for mature IGF-1 (~7 kDa). (D) Representative immunoblotting and (E) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (C) or two-way ANOVA followed by Tukey's multiple comparison post hoc tests (A, E). *Significantly different compared to CTR; #Significantly different compared to WT mice; * and # p ≤ .05; ** p ≤ .01 *** and ### p ≤ .001.

    Journal: The FASEB Journal

    Article Title: Impaired myoblast differentiation and muscle IGF‐1 receptor signaling pathway activation after N‐glycosylation inhibition

    doi: 10.1096/fj.202400213rr

    Figure Lengend Snippet: FIGURE 4 IGF-1 production and IGF1R signaling pathway activation in TA muscle of WT and MLC/mIgf-1 mice treatment with low TUN dose (0.1 mg/kg of TUN for 15 days). (A) Expression of endogenous Igf-1 mRNA isoforms (i.e., Igf-1Ea and Igf-1Ec mRNAs) and total Igf-1 (i.e., endogenous and mIgf-1 transgene mRNAs) in the TA muscle of WT (n = 3) and MLC/mIgf-1 (n = 3) mice treated with TUN. (B) Representative immunoblotting and (C) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using an antibody directed against mature mouse IGF-1 sequence. Three bands at a molecular weight of ~22, ~17, and ~12 kDa were detected in TA muscle of MLC/ mIgf1 mice. Recombinant mouse IGF-1 mature protein was loaded as a positive control for mature IGF-1 (~7 kDa). (D) Representative immunoblotting and (E) band densitometry analysis of TA muscle of WT and MLC/mIgf1 mice using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (C) or two-way ANOVA followed by Tukey's multiple comparison post hoc tests (A, E). *Significantly different compared to CTR; #Significantly different compared to WT mice; * and # p ≤ .05; ** p ≤ .01 *** and ### p ≤ .001.

    Article Snippet: Primary antibodies against phospho- IGF1R β (1:2000; cat. n. 3024 Cell Signaling Technology), total IGF1R β (1:2000; cat. n. 3027 Cell Signaling Technology), phospho- Akt (Ser473) (1:2000; cat. n. 9271 Cell Signaling Technology), total Akt (1:2000; cat. n. 9272 Cell Signaling Technology), phospho- p44/42 (ERK1/2) (1:2000; cat. n. 9101 Cell Signaling Technology), total p44/42 (ERK1/2) (1:2000; cat. n. 9102 Cell Signaling Technology), PCNA (1:5000, cat. n. MAB 424R Millipore), MF20 (1:500, DSHB), and mouse/rat biotinylated IGF- 1 antibody (1:300, cat. n. BAF791 R&D Systems) were incubated overnight at 4°C.

    Techniques: Activation Assay, Expressing, Western Blot, Sequencing, Molecular Weight, Recombinant, Positive Control, Comparison

    FIGURE 5 Effect of TUN treatment on IGF1R production and IGF1R signaling pathway activation in C2C12. (A) IGF1R and IGF1R proreceptor production in C2C12 cells treated with 0.01 μg/mL of TUN and harvested at day 1. (B) Immunofluorescence analysis of C2C12 cells stained with ant-IGF1R and DAPI, the scale bar represents 200 μm. (C) Representative immunoblotting and (D) band densitometry analysis of IGF-1-induced IGF-1R signaling pathway activation in CTR- and TUN-treated C2C12 cells using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. The calculation of pIGF1R level was normalized against total lysed protein instead of total IGF1R to account for the marked reduction of total IGF1R after TUN treatment. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (A) or one-way ANOVA followed by Tukey's multiple comparison post hoc tests (D). *Significantly different compared to CTR, #Significantly different compared to IGF-1-treated cells; ** p ≤ .01, *** p ≤ .001; ## p ≤ .01, ### p ≤ .001.

    Journal: The FASEB Journal

    Article Title: Impaired myoblast differentiation and muscle IGF‐1 receptor signaling pathway activation after N‐glycosylation inhibition

    doi: 10.1096/fj.202400213rr

    Figure Lengend Snippet: FIGURE 5 Effect of TUN treatment on IGF1R production and IGF1R signaling pathway activation in C2C12. (A) IGF1R and IGF1R proreceptor production in C2C12 cells treated with 0.01 μg/mL of TUN and harvested at day 1. (B) Immunofluorescence analysis of C2C12 cells stained with ant-IGF1R and DAPI, the scale bar represents 200 μm. (C) Representative immunoblotting and (D) band densitometry analysis of IGF-1-induced IGF-1R signaling pathway activation in CTR- and TUN-treated C2C12 cells using antibodies directed against phosphorylated (pIGF1R) and total IGF1R, phosphorylated (pAKT) and total AKT, and phosphorylated (pERK1/2) and total ERK1/2. The calculation of pIGF1R level was normalized against total lysed protein instead of total IGF1R to account for the marked reduction of total IGF1R after TUN treatment. All bar charts are presented as mean values ± SD. Significant differences were determined using unpaired t-test (A) or one-way ANOVA followed by Tukey's multiple comparison post hoc tests (D). *Significantly different compared to CTR, #Significantly different compared to IGF-1-treated cells; ** p ≤ .01, *** p ≤ .001; ## p ≤ .01, ### p ≤ .001.

    Article Snippet: Primary antibodies against phospho- IGF1R β (1:2000; cat. n. 3024 Cell Signaling Technology), total IGF1R β (1:2000; cat. n. 3027 Cell Signaling Technology), phospho- Akt (Ser473) (1:2000; cat. n. 9271 Cell Signaling Technology), total Akt (1:2000; cat. n. 9272 Cell Signaling Technology), phospho- p44/42 (ERK1/2) (1:2000; cat. n. 9101 Cell Signaling Technology), total p44/42 (ERK1/2) (1:2000; cat. n. 9102 Cell Signaling Technology), PCNA (1:5000, cat. n. MAB 424R Millipore), MF20 (1:500, DSHB), and mouse/rat biotinylated IGF- 1 antibody (1:300, cat. n. BAF791 R&D Systems) were incubated overnight at 4°C.

    Techniques: Activation Assay, Immunofluorescence, Staining, Western Blot, Comparison