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>   home   >   Products   >   Primary Antibodies   >   Stem Cells   >   IGF1R antibody - middle region   

IGF1R antibody - middle region

Rabbit Polyclonal Antibody

     
  • IHC - IGF1R antibody - middle region AI16163
    mouse skelatal muscle
  • WB - IGF1R antibody - middle region AI16163

    WB Suggested Anti-IGF1R Antibody Titration: 0.2-1 μg/ml
    ELISA Titer: 1:312500
    Positive Control: Jurkat cell lysate
  • SPECIFICATION
  • CITATIONS
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Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
WB, IHC
Primary Accession P08069
Other Accession NM_000875, NP_000866
Reactivity Human, Mouse, Rat, Pig, Sheep, Horse, Bovine, Dog
Predicted Human, Mouse, Rat, Pig, Chicken, Sheep, Horse, Bovine, Dog
Host Rabbit
Clonality Polyclonal
Calculated MW 71kDa
Additional Information
Gene ID 3480
Alias Symbol CD221, IGFIR, JTK13, MGC142170, MGC142172, MGC18216, IGFR
Other Names Insulin-like growth factor 1 receptor, 2.7.10.1, Insulin-like growth factor I receptor, IGF-I receptor, CD221, Insulin-like growth factor 1 receptor alpha chain, Insulin-like growth factor 1 receptor beta chain, IGF1R
Target/Specificity Directed to the beta chain of IGF1R
Format Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Reconstitution & Storage Add 50 ul of distilled water. Final anti-IGF1R antibody concentration is 1 mg/ml in PBS buffer with 2% sucrose. For longer periods of storage, store at 20°C. Avoid repeat freeze-thaw cycles.
PrecautionsIGF1R antibody - middle region is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name IGF1R
Function Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with a lower affinity. The activated IGF1R is involved in cell growth and survival control. IGF1R is crucial for tumor transformation and survival of malignant cell. Ligand binding activates the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway. The result of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD. In parallel to PI3K- driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins. In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R. IGF1 exerts inhibiting activities on JNK activation via phosphorylation and inhibition of MAP3K5/ASK1, which is able to directly associate with the IGF1R.
Cellular Location Cell membrane; Single-pass type I membrane protein
Tissue Location Found as a hybrid receptor with INSR in muscle, heart, kidney, adipose tissue, skeletal muscle, hepatoma, fibroblasts, spleen and placenta (at protein level). Expressed in a variety of tissues. Overexpressed in tumors, including melanomas, cancers of the colon, pancreas prostate and kidney
Research Areas
Citations (0)

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Background

Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with a lower affinity. The activated IGF1R is involved in cell growth and survival control. IGF1R is crucial for tumor transformation and survival of malignant cell. Ligand binding activates the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway. The result of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD. In parallel to PI3K- driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins. In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R. IGF1 exerts inhibiting activities on JNK activation via phosphorylation and inhibition of MAP3K5/ASK1, which is able to directly associate with the IGF1R.

References

Ullrich A.,et al.EMBO J. 5:2503-2512(1986).
Abbot A.M.,et al.J. Biol. Chem. 267:10759-10763(1992).
Nagase T.,et al.Submitted (FEB-2008) to the EMBL/GenBank/DDBJ databases.
Zody M.C.,et al.Nature 440:671-675(2006).
Cooke D.W.,et al.Biochem. Biophys. Res. Commun. 177:1113-1120(1991).

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$ 293.00
Cat# AI16163
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