Reactive species
Human; Mouse;Rat
Antibody type
Polyclonal Antibody
Protein name
TGFBR2 (Phospho-Tyr284)
Immunogen
Synthesized peptide derived from human TGFBR2 (Phospho-Tyr284)
Specificity
This antibody detects endogenous levels of TGFBR2 (Phospho-Tyr284) at Human, Mouse,Rat
Constitute
Liquid in PBS containing 50% glycerol, and 0.125% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
WB 1:500-2000
Purification process
The antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen.
Other name
TGF-beta receptor type-2 (TGFR-2) (EC 2.7.11.30) (TGF-beta type II receptor) (Transforming growth factor-beta receptor type II) (TGF-beta receptor type II) (TbetaR-II)
Background
This gene encodes a member of the Ser/Thr protein kinase family and the TGFB receptor subfamily. The encoded protein is a transmembrane protein that has a protein kinase domain, forms a heterodimeric complex with another receptor protein, and binds TGF-beta. This receptor/ligand complex phosphorylates proteins, which then enter the nucleus and regulate the transcription of a subset of genes related to cell proliferation. Mutations in this gene have been associated with Marfan Syndrome, Loeys-Deitz Aortic Aneurysm Syndrome, and the development of various types of tumors. Alternatively spliced transcript variants encoding different isoforms have been characterized. [provided by RefSeq, Jul 2008],
Function
catalytic activity:ATP + [receptor-protein] = ADP + [receptor-protein] phosphate.,cofactor:Magnesium or manganese.,disease:Defects in TGFBR2 are a cause of esophageal cancer [MIM:133239].,disease:Defects in TGFBR2 are the cause of aortic aneurysm familial thoracic type 3 (AAT3) [MIM:610380]. Aneurysms and dissections of the aorta usually result from degenerative changes in the aortic wall. Thoracic aortic aneurysms and dissections are primarily associated with a characteristic histologic appearance known as 'medial necrosis' or 'Erdheim cystic medial necrosis' in which there is degeneration and fragmentation of elastic fibers, loss of smooth muscle cells, and an accumulation of basophilic ground substance. AAT3 is an autosomal dominant disorder with reduced penetrance and variable expression.,disease:Defects in TGFBR2 are the cause of hereditary non-polyposis colorectal cancer type 6 (HN
