Thermo Fisher Scientific Phospho-IGF1R (Tyr1165, Tyr1166) Polyclonal Antibody

Applications

Tested Dilution

Publications

Flow Cytometry (Flow)

1:20-1:100

-

ELISA (ELISA)

1:500-1:1,000

-

Product Specifications

Species Reactivity

Human, Mouse, Rat

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

KLH conjugated synthetic phosphopeptide derived from human IGF1R around the phosphorylation site of Tyr1165+Tyr1166. if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:IGF1R (CD221),uniProtId:P08069-1,ncbiNodeId:9606,antigenRange:1165,antigenLength:1367,antigenImageFileName:BS-5449R_IGF1R_CD221_P08069-1_Rabbit.svg,antigenImageFileNamePDP:BS-5449R_IGF1R_CD221_P08069-1_Rabbit_PDP.jpeg,sortOrder:1}\]; $mangular.isB2BCMGT = false; $mangular.isEpitopesModalImageMultiSizeEnabled = true;

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Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

1 mg/mL

Purification

Protein A

Storage buffer

0.01M TBS, pH 7.4, with 50% glycerol, 1% BSA

Contains

0.02% ProClin 300

Storage conditions

-20°C

Shipping conditions

Ambient (domestic); Wet ice (international)

Target Information

IGF1R, also known as Insulin-like Growth Factor 1 (IGF-1) Receptor, is a receptor tyrosine kinase activated by IGF-1 and IGF-2. IGFR has been implicated in a variety of cancers. The protein is a tetramer consisting of two alpha, and two beta subunits. The alpha-subunits binds to insulin growth factor 1 with higher affinity than to insulin growth factor 2. Binding results in a conformational change, followed by autophosphorylation of IGF-1R at positions 1134, 1135, 1136. The activated IGF-1R in turn, causes phosphorylation of substrate proteins, followed by sequential activation of RAS, RAF, and mitogen-activated protein kinase isoforms ERK, p38, and JNK, leading to the transcription of genes that drive proliferation.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.