Rabbit Anti-TGFBR2 Recombinant Antibody (CBYJT-2807) (CBMAB-T2031-YJ)

TGFBR2 Gene(Protein Coding) Transforming Growth Factor Beta Receptor 2

TGFBR2 is a transmembrane protein that has a protein kinase domain, forms a heterodimeric complex with TGF-beta receptor type-1, and binds TGF-beta. It/ligand complex phosphorylates proteins, which then enter the nucleus and regulate the transcription of genes related to cell proliferation, cell cycle arrest, wound healing, immunosuppression, and tumorigenesis. Mutations in this gene have been associated with Marfan Syndrome, Loeys-Deitz Aortic Aneurysm Syndrome, and the development of various types of tumors.

Transforming Growth Factor Beta Receptor 2; Transforming Growth Factor, Beta Receptor II (70/80kDa); Transforming Growth Factor Beta Receptor II; TGF-Beta Type II Receptor; EC 2.7.11.30; TbetaR-II; TGFR-2; Transforming Growth Factor, Beta Receptor II Epsilon; Transforming Growth Factor, Beta Receptor II Alpha; Transforming Growth Factor, Beta Receptor II Delta; Transforming Growth Factor, Beta Receptor II Gamma; Transforming Growth Factor Beta Receptor Type IIC; Transforming Growth Factor, Beta Receptor II Beta; Transforming Growth Factor-Beta Receptor Type II; TGF-Beta Receptor Type IIB

Transmembrane serine/threonine kinase forming with the TGF-beta type I serine/threonine kinase receptor, TGFBR1, the non-promiscuous receptor for the TGF-beta cytokines TGFB1, TGFB2 and TGFB3. Transduces the TGFB1, TGFB2 and TGFB3 signal from the cell surface to the cytoplasm and thus regulates a plethora of physiological and pathological processes including cell cycle arrest in epithelial and hematopoietic cells, control of mesenchymal cell proliferation and differentiation, wound healing, extracellular matrix production, immunosuppression and carcinogenesis. The formation of the receptor complex composed of 2 TGFBR1 and 2 TGFBR2 molecules symmetrically bound to the cytokine dimer results in the phosphorylation and activation of TGFBR1 by the constitutively active TGFBR2. Activated TGFBR1 phosphorylates SMAD2 which dissociates from the receptor and interacts with SMAD4. The SMAD2-SMAD4 complex is subsequently translocated to the nucleus where it modulates the transcription of the TGF-beta-regulated genes. This constitutes the canonical SMAD-dependent TGF-beta signaling cascade. Also involved in non-canonical, SMAD-independent TGF-beta signaling pathways.
Isoform 1
Has transforming growth factor beta-activated receptor activity.
Isoform 2
Has transforming growth factor beta-activated receptor activity.
Isoform 3
Binds TGFB1, TGFB2 and TGFB3 in the picomolar affinity range without the participation of additional receptors. Blocks activation of SMAD2 and SMAD3 by TGFB1.

Biological Process activation of protein kinase activitySource:BHF-UCL
Biological Process agingSource:Ensembl
Biological Process animal organ regenerationSource:Ensembl
Biological Process apoptotic processSource:UniProtKB1 Publication
Biological Process atrioventricular valve morphogenesisSource:BHF-UCL
Biological Process blood vessel developmentSource:BHF-UCL1 Publication
Biological Process brain developmentSource:BHF-UCL
Biological Process branching involved in blood vessel morphogenesisSource:BHF-UCL
Biological Process bronchus morphogenesisSource:Ensembl
Biological Process cardiac left ventricle morphogenesisSource:BHF-UCL
Biological Process cellular response to growth factor stimulusSource:GO_Central1 Publication
Biological Process common-partner SMAD protein phosphorylationSource:Ensembl
Biological Process digestive tract developmentSource:Ensembl
Biological Process embryo implantationSource:Ensembl
Biological Process embryonic cranial skeleton morphogenesisSource:BHF-UCL
Biological Process embryonic hemopoiesisSource:BHF-UCL
Biological Process endocardial cushion fusionSource:BHF-UCL
Biological Process gastrulationSource:Ensembl
Biological Process growth plate cartilage chondrocyte growthSource:Ensembl
Biological Process heart developmentSource:BHF-UCL
Biological Process heart loopingSource:BHF-UCL
Biological Process in utero embryonic developmentSource:Ensembl
Biological Process inferior endocardial cushion morphogenesisSource:BHF-UCL
Biological Process Langerhans cell differentiationSource:Ensembl
Biological Process lens development in camera-type eyeSource:Ensembl
Biological Process lens fiber cell apoptotic processSource:Ensembl
Biological Process lung lobe morphogenesisSource:Ensembl
Biological Process mammary gland morphogenesisSource:Ensembl
Biological Process membranous septum morphogenesisSource:BHF-UCL
Biological Process miRNA transportSource:BHF-UCL
Biological Process myeloid dendritic cell differentiationSource:BHF-UCL
Biological Process negative regulation of cardiac muscle cell proliferationSource:Ensembl
Biological Process Notch signaling pathwaySource:Ensembl
Biological Process outflow tract morphogenesisSource:BHF-UCL
Biological Process outflow tract septum morphogenesisSource:BHF-UCL
Biological Process pathway-restricted SMAD protein phosphorylationSource:BHF-UCL1 Publication
Biological Process peptidyl-serine phosphorylationSource:BHF-UCL1 Publication
Biological Process peptidyl-threonine phosphorylationSource:BHF-UCL1 Publication
Biological Process positive regulation of angiogenesisSource:Ensembl
Biological Process positive regulation of B cell tolerance inductionSource:BHF-UCL
Biological Process positive regulation of CD4-positive, alpha-beta T cell proliferationSource:BHF-UCL1 Publication
Biological Process positive regulation of cell population proliferationSource:ProtInc1 Publication
Biological Process positive regulation of epithelial cell migrationSource:Ensembl
Biological Process positive regulation of epithelial to mesenchymal transitionSource:BHF-UCL1 Publication
Biological Process positive regulation of epithelial to mesenchymal transition involved in endocardial cushion formationSource:BHF-UCL
Biological Process positive regulation of mesenchymal cell proliferationSource:BHF-UCL
Biological Process positive regulation of NK T cell differentiationSource:BHF-UCL
Biological Process positive regulation of pathway-restricted SMAD protein phosphorylationSource:ComplexPortal1 Publication
Biological Process positive regulation of reactive oxygen species metabolic processSource:BHF-UCL1 Publication
Biological Process positive regulation of skeletal muscle tissue regenerationSource:Ensembl
Biological Process positive regulation of smooth muscle cell proliferationSource:Ensembl
Biological Process positive regulation of T cell tolerance inductionSource:BHF-UCL
Biological Process positive regulation of tolerance induction to self antigenSource:BHF-UCL
Biological Process protein phosphorylationSource:BHF-UCL1 Publication
Biological Process receptor-mediated endocytosisSource:Ensembl
Biological Process regulation of cell population proliferationSource:BHF-UCL
Biological Process regulation of gene expressionSource:Ensembl
Biological Process regulation of stem cell proliferationSource:Ensembl
Biological Process response to cholesterolSource:BHF-UCL1 Publication
Biological Process response to estrogenSource:Ensembl
Biological Process response to glucoseSource:Ensembl
Biological Process response to hypoxiaSource:Ensembl
Biological Process response to mechanical stimulusSource:Ensembl
Biological Process response to nutrientSource:Ensembl
Biological Process response to steroid hormoneSource:Ensembl
Biological Process response to xenobiotic stimulusSource:BHF-UCL1 Publication
Biological Process secondary palate developmentSource:BHF-UCL
Biological Process smoothened signaling pathwaySource:Ensembl
Biological Process trachea formationSource:Ensembl
Biological Process transforming growth factor beta receptor signaling pathwaySource:BHF-UCL1 Publication
Biological Process tricuspid valve morphogenesisSource:BHF-UCL
Biological Process vasculogenesisSource:BHF-UCL
Biological Process ventricular septum morphogenesisSource:BHF-UCL
Biological Process wound healingSource:Ensembl

Cell membrane
Membrane raft
Isoform 3
Secreted

Hereditary non-polyposis colorectal cancer 6 (HNPCC6):
An autosomal dominant disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early-onset colorectal carcinoma (CRC) and extra-colonic tumors of the gastrointestinal, urological and female reproductive tracts. HNPCC is reported to be the most common form of inherited colorectal cancer in the Western world. Clinically, HNPCC is often divided into two subgroups. Type I is characterized by hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II is characterized by increased risk for cancers in certain tissues such as the uterus, ovary, breast, stomach, small intestine, skin, and larynx in addition to the colon. Diagnosis of classical HNPCC is based on the Amsterdam criteria: 3 or more relatives affected by colorectal cancer, one a first degree relative of the other two; 2 or more generation affected; 1 or more colorectal cancers presenting before 50 years of age; exclusion of hereditary polyposis syndromes. The term 'suspected HNPCC' or 'incomplete HNPCC' can be used to describe families who do not or only partially fulfill the Amsterdam criteria, but in whom a genetic basis for colon cancer is strongly suspected.
Esophageal cancer (ESCR):
A malignancy of the esophagus. The most common types are esophageal squamous cell carcinoma and adenocarcinoma. Cancer of the esophagus remains a devastating disease because it is usually not detected until it has progressed to an advanced incurable stage.
Loeys-Dietz syndrome 2 (LDS2):
An aortic aneurysm syndrome with widespread systemic involvement, characterized by arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Physical findings include prominent joint laxity, easy bruising, wide and atrophic scars, velvety and translucent skin with easily visible veins, spontaneous rupture of the spleen or bowel, and catastrophic complications of pregnancy, including rupture of the gravid uterus and the arteries, either during pregnancy or in the immediate postpartum period. Some patients have craniosynostosis, exotropy, micrognathia and retrognathia, structural brain abnormalities, and intellectual deficit.

Extracellular: 23-166
Helical: 167-187
Cytoplasmic: 188-567

Phosphorylated on a Ser/Thr residue in the cytoplasmic domain.