IGF-1Rβ Antibody [G20F1] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IHC1:400

Application
WB, IHC

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
95 kDa, 200 kDa

Positive Control	Human breast carcinoma; Human papillary serous cystadenocarcinoma of the ovary; Human prostate adenocarcinoma; Human squamous cell carcinoma; Human papillary thyroid carcinoma; MCF7 cells; 293 cells
Negative Control	SK-UT-1 cells

Datasheet & SDS

Biological Description

Specificity
IGF-1Rβ Antibody [G20F1] detects endogenous levels of total IGF-1Rβ protein.

Clone
G20F1

Synonym(s)
Insulin-like growth factor 1 receptor; Insulin-like growth factor I receptor (IGF-I receptor); CD221; IGF1R

Background
The IGF-1Rβ subunit constitutes the cytoplasmic, catalytic core of the type I insulin-like growth factor receptor (IGF-1R), a transmembrane receptor tyrosine kinase (RTK) heterotetramer (α2β2) that is structurally and functionally similar to the insulin receptor. IGF-1R is ubiquitously expressed in fetal and postnatal tissues, mediating growth signals from IGF-I and IGF-II ligands. Its modular design includes a short extracellular segment connected to the transmembrane helix, a juxtamembrane region, a central bilobal kinase domain (residues ~970–1255) with a conserved activation loop containing three key tyrosines (Tyr1131, Tyr1135, Tyr1136), the primary autophosphorylation sites critical for full kinase activation, and a C-terminal tail with docking motifs for adaptor proteins such as IRS-1/2 and Shc. Upon ligand binding, conformational changes in the α-subunit facilitate β-to-β trans-autophosphorylation at these tyrosines, which activates the intrinsic kinase activity to phosphorylate downstream substrates. This triggers the PI3K/Akt and MAPK/ERK pathways, driving cell proliferation, survival, differentiation, and metabolic regulation, and plays essential roles in somatic growth (in concert with growth hormone) and developmental patterning. Hyperactivation of IGF-1Rβ promotes oncogenesis in various cancers, such as breast and prostate, by enhancing mitogenic signaling and resistance to apoptosis, while knockdown can reverse malignant traits and increase therapy sensitivity. IGF-1Rβ is also implicated in metabolic disorders like diabetes, and elevated levels are a prognostic marker in cancer.

Background

The IGF-1Rβ subunit constitutes the cytoplasmic, catalytic core of the type I insulin-like growth factor receptor (IGF-1R), a transmembrane receptor tyrosine kinase (RTK) heterotetramer (α2β2) that is structurally and functionally similar to the insulin receptor. IGF-1R is ubiquitously expressed in fetal and postnatal tissues, mediating growth signals from IGF-I and IGF-II ligands. Its modular design includes a short extracellular segment connected to the transmembrane helix, a juxtamembrane region, a central bilobal kinase domain (residues ~970–1255) with a conserved activation loop containing three key tyrosines (Tyr1131, Tyr1135, Tyr1136), the primary autophosphorylation sites critical for full kinase activation, and a C-terminal tail with docking motifs for adaptor proteins such as IRS-1/2 and Shc. Upon ligand binding, conformational changes in the α-subunit facilitate β-to-β trans-autophosphorylation at these tyrosines, which activates the intrinsic kinase activity to phosphorylate downstream substrates. This triggers the PI3K/Akt and MAPK/ERK pathways, driving cell proliferation, survival, differentiation, and metabolic regulation, and plays essential roles in somatic growth (in concert with growth hormone) and developmental patterning. Hyperactivation of IGF-1Rβ promotes oncogenesis in various cancers, such as breast and prostate, by enhancing mitogenic signaling and resistance to apoptosis, while knockdown can reverse malignant traits and increase therapy sensitivity. IGF-1Rβ is also implicated in metabolic disorders like diabetes, and elevated levels are a prognostic marker in cancer.

References
https://pubmed.ncbi.nlm.nih.gov/31594955/ https://pubmed.ncbi.nlm.nih.gov/10961344/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%