TGF beta Receptor II protein (Fc Chimera) (ab83578)
Constituents: 10% Trehalose, 1% Human serum albumin
Our Abpromise guarantee covers the use of ab83578 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
ab83578 migrates as a broad band between 45 and 70 kDa in SDS-PAGE due to post-translation modifications, in particular glycosylation. This compares with the unmodified TGF beta Receptor II-Fc Chimera that has a predicted molecular mass of 42.7kDa. ab83578 consists of 5-40% carbohydrate by weight.
ab83578 separates into a number of isoforms with a pI between 4.7 and 7.2 in 2D PAGE due to post-translational modifications, in particular glycosylation. This compares with the unmodified TGF beta Receptor II-Fc Chimera that has a predicted pI of 6.22.
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
- LDS2BMFS2RIICTAAD2TbetaR IITbetaR-IITGF beta receptor type IITGF beta receptor type IIBTGF beta type II receptorTGF-beta receptor type IITGF-beta receptor type-2TGF-beta type II receptorTGFB R2TGFbeta RIITGFBR2TGFR-2TGFR2_HUMANTransforming growth factor beta receptor IITransforming growth factor beta receptor type IITransforming growth factor beta receptor type IICTransforming growth factor-beta receptor type II
Defects in TGFBR2 are a cause of esophageal cancer (ESCR) [MIM:133239].
Defects in TGFBR2 are the cause of Loeys-Dietz syndrome type 1B (LDS1B) [MIM:610168]. LDS1 is an aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by arterial tortuosity and aneurysms, craniosynostosis, hypertelorism, and bifid uvula or cleft palate. Other findings include exotropy, micrognathia and retrognathia, structural brain abnormalities, intellectual deficit, congenital heart disease, translucent skin, joint hyperlaxity and aneurysm with dissection throughout the arterial tree.
Defects in TGFBR2 are the cause of Loeys-Dietz syndrome type 2B (LDS2B) [MIM:610380]. An aortic aneurysm syndrome with widespread systemic involvement. 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, diffuse arterial aneurysms and dissections, and catastrophic complications of pregnancy, including rupture of the gravid uterus and the arteries, either during pregnancy or in the immediate postpartum period. LDS2 is characterized by the absence of craniofacial abnormalities with the exception of bifid uvula that can be present in some patients. Note=TGFBR2 mutations Cys-460 and His-460 have been reported to be associated with thoracic aortic aneurysms and dissection (TAAD). This phenotype, also known as thoracic aortic aneurysms type 3 (AAT3), is distinguised from LDS2B by having aneurysms restricted to thoracic aorta. As individuals carrying these mutations also exhibit descending aortic disease and aneurysms of other arteries (PubMed:16027248), they have been considered as LDS2B by the OMIM resource.
Contains 1 protein kinase domain.
modificationsPhosphorylated on a Ser/Thr residue in the cytoplasmic domain.
TGF beta Receptor II protein (Fc Chimera) images
The densitometry scan demonstrates the purified human cell expressed protein exists in multiple isoforms, which differ according to their level of post-translational modification. The triangle indicates theoretical pI and MW of the protein.
References for TGF beta Receptor II protein (Fc Chimera) (ab83578)
ab83578 has not yet been referenced specifically in any publications.