IGF1R anticorps (C-Term)

N° du produit ABIN6262491

L’anticorps Lapin Polyclonal anti-IGF1R a été validé pour WB, IHC, ELISA, IF et ICC. Il convient pour détecter IGF1R dans des échantillons de Humain, Souris et Rat.

Aperçu rapide pour IGF1R anticorps (C-Term) (ABIN6262491)

Antigène: IGF1R (Insulin-Like Growth Factor 1 Receptor (IGF1R))

Reactivité: Humain, Souris, Rat

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp IGF1R est non-conjugé

Application: Western Blotting (WB), Immunohistochemistry (IHC), ELISA, Immunofluorescence (IF), Immunocytochemistry (ICC)

Détail du produit anti-IGF1R anticorps

Épitope: C-Term

Specificité: IGF1R/Insulin Receptor Antibody detects endogenous levels of total IGF1R/Insulin Receptor.

Homologie: Bovine,Rabbit,Dog,Chicken,Xenopus

Purification: The antiserum was purified by peptide affinity chromatography using SulfoLink^TM Coupling Resin (Thermo Fisher Scientific).

Immunogène: A synthesized peptide derived from human IGF1R/Insulin Receptor, corresponding to a region within C-terminal amino acids.

Isotype: IgG

Information d'application

Indications d'application: WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000

Restrictions: For Research Use only

Stockage

Format: Liquid

Concentration: 1 mg/mL

Buffer: Rabbit IgG in phosphate buffered saline , pH 7.4, 150 mM NaCl, 0.02 % sodium azide and 50 % glycerol.

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Stock: -20 °C

Stockage commentaire: Store at -20 °C. Stable for 12 months from date of receipt.

Date de péremption: 12 months

Détails sur IGF1R

Antigène: IGF1R (Insulin-Like Growth Factor 1 Receptor (IGF1R))

Autre désignation: IGF1R,INSR

Sujet:

Description: 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.

Gene: IGF1R

Poids moléculaire: 90,155kDa

ID gène: 3480, 3643

UniProt: P08069, P06213

Pathways: Signalisation RTK, Regulation of Hormone Metabolic Process, Regulation of Hormone Biosynthetic Process, Autophagy