IGF1R Antikörper (C-Term)

Produktnummer ABIN6262491

Der Kaninchen Polyklonal Anti-IGF1R-Antikörper wurde für WB, IHC, ELISA, IF und ICC validiert. Er ist geeignet, IGF1R in Proben von Human, Maus und Ratte zu detektieren.

Kurzübersicht für IGF1R Antikörper (C-Term) (ABIN6262491)

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

Reaktivität: Human, Maus, Ratte

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Dieser IGF1R Antikörper ist unkonjugiert

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

Produktdetails anti-IGF1R Antikörper

Bindungsspezifität: C-Term

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

Homologie: Bovine,Rabbit,Dog,Chicken,Xenopus

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

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

Isotyp: IgG

Anwendungsinformationen

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

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: 1 mg/mL

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

Konservierungsmittel: Sodium azide

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

Lagerung: -20 °C

Informationen zur Lagerung: Store at -20 °C. Stable for 12 months from date of receipt.

Haltbarkeit: 12 months

Details zu IGF1R

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

Andere Bezeichnung: IGF1R,INSR

Hintergrund:

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

Molekulargewicht: 90,155kDa

Gen-ID: 3480, 3643

UniProt: P08069, P06213

Pathways: RTK Signalweg, Regulation of Hormone Metabolic Process, Regulation of Hormone Biosynthetic Process, Autophagie