Key features and details
- Rabbit polyclonal to TGF beta Receptor I (phospho S165)
- Suitable for: ICC/IF
- Reacts with: Human
- Isotype: IgG
Product nameAnti-TGF beta Receptor I (phospho S165) antibody
See all TGF beta Receptor I primary antibodies
DescriptionRabbit polyclonal to TGF beta Receptor I (phospho S165)
Tested applicationsSuitable for: ICC/IFmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
- HeLa cells.
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Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: 50% Glycerol, 0.88% Sodium chloride, 49% PBS
Concentration information loading...
PurityImmunogen affinity purified
Purification notesab112095 is affinity-purified from rabbit antiserum by affinity-chromatography using an epitope-specific phosphopeptide. The antibody against non-phosphopeptide was removed by chromatography using non-phosphopeptide corresponding to the phosphorylation site.
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab112095 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/100 - 1/500.
1/100 - 1/500.
FunctionOn ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for TGF-beta.
Tissue specificityFound in all tissues examined, most abundant in placenta and least abundant in brain and heart.
Involvement in diseaseDefects in TGFBR1 are the cause of Loeys-Dietz syndrome type 1A (LDS1A) [MIM:609192]; also known as Furlong syndrome or Loeys-Dietz aortic aneurysm syndrome (LDAS). 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 TGFBR1 are the cause of Loeys-Dietz syndrome type 2A (LDS2A) [MIM:608967]. LDS2 is 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.
Defects in TGFBR1 are the cause of aortic aneurysm familial thoracic type 5 (AAT5) [MIM:608967]. 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' in which there is degeneration and fragmentation of elastic fibers, loss of smooth muscle cells, and an accumulation of basophilic ground substance.
Sequence similaritiesBelongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. TGFB receptor subfamily.
Contains 1 GS domain.
Contains 1 protein kinase domain.
modificationsPhosphorylated at basal levels in the absence of ligand binding. Activated by multiple phosphorylation, mainly in the GS region.
- Information by UniProt
- AAT 5 antibody
- AAT5 antibody
- Activin A receptor type II like kinase 53kDa antibody
ab112095 has been referenced in 8 publications.
- Lou LL et al. (+)-Isobicyclogermacrenal and spathulenol from Aristolochia yunnanensis alleviate cardiac fibrosis by inhibiting transforming growth factor ß/small mother against decapentaplegic signaling pathway. Phytother Res 33:214-223 (2019). PubMed: 30375049
- Wojciech S et al. The orphan GPR50 receptor promotes constitutive TGFß receptor signaling and protects against cancer development. Nat Commun 9:1216 (2018). PubMed: 29572483
- Dalvi P et al. Hyperactive TGF-ß Signaling in Smooth Muscle Cells Exposed to HIV-protein(s) and Cocaine: Role in Pulmonary Vasculopathy. Sci Rep 7:10433 (2017). WB . PubMed: 28874783
- Liu Y et al. Decorin inhibits the proliferation of HepG2 cells by elevating the expression of transforming growth factor-ß receptor II. Exp Ther Med 12:2191-2195 (2016). WB ; Human . PubMed: 27698710
- Jin K et al. Hepatic Premalignant Alterations Triggered by Human Nephrotoxin Aristolochic Acid I in Canines. Cancer Prev Res (Phila) 9:324-34 (2016). PubMed: 26851235
- Su CT et al. Latent transforming growth factor binding protein 4 regulates transforming growth factor beta receptor stability. Hum Mol Genet 24:4024-36 (2015). PubMed: 25882708
- Silva MT et al. Impaired structural and functional regeneration of skeletal muscles from ß2-adrenoceptor knockout mice. Acta Physiol (Oxf) 211:617-33 (2014). PubMed: 24938737
- Rudalska R et al. In vivo RNAi screening identifies a mechanism of sorafenib resistance in liver cancer. Nat Med 20:1138-46 (2014). PubMed: 25216638