igf1r primary antibody  (Novus Biologicals)

Journal: Endocrinology

Article Title: IGF1 Signaling Regulates Neuropeptide Expression in Hypothalamic Neurons Under Physiological and Pathological Conditions

doi: 10.1210/endocr/bqaf051

Figure Lengend Snippet: List of antibodies for Western blots

Article Snippet: IGF1R-β Primary Antibody , Cell Signaling Technology , 3027 RRID:AB_2122378.

Techniques: Western Blot

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

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

Journal: Biomedicines

Article Title: MicroRNA Associated with the Invasive Phenotype in Clear Cell Renal Cell Carcinoma: Let-7c-5p Inhibits Proliferation, Migration, and Invasion by Targeting Insulin-like Growth Factor 1 Receptor.

doi: 10.3390/biomedicines10102425

Figure Lengend Snippet: Figure 3. The effect of let-7c-5p on the expression of IGF1R. (A) Relative luciferase activity of Caki-1 cells for each vector, including mutants, transfected with pre-let-7c-5p, relative to the negative control transfectant (predicted sites detailed in the inset below the chart). (B) Relative expression of IGF1R in Caki-1 and 786-O cells transfected with let-7c-5p after 48 h, relative to the negative control for each cell line. Representative image inset to the right: the first lane of each pair corresponds to IGF1R and the second is total protein detected for the same lane. * p < 0.05, ** p < 0.01, and NS = not significant.

Article Snippet: IGF1R primary antibody (NBP1-77679, Novus Biologicals, Littleton, CO, USA) at a concentration of 1:25 diluted in Antibody diluent 2 (ProteinSimple) and rabbit secondary antibody (042-206, ProteinSimple, used as provided) were added according to the manufacturer’s protocol.

Techniques: Expressing, Luciferase, Activity Assay, Plasmid Preparation, Transfection, Negative Control