Key features and details
- Rabbit polyclonal to TGF beta Receptor II
- Suitable for: ICC/IF, WB, IHC-P
- Reacts with: Mouse, Rat, Human
- Isotype: IgG
Product nameAnti-TGF beta Receptor II antibody
See all TGF beta Receptor II primary antibodies
DescriptionRabbit polyclonal to TGF beta Receptor II
Tested applicationsSuitable for: ICC/IF, WB, IHC-Pmore details
Species reactivityReacts with: Mouse, Rat, Human
Recombinant fragment within Human TGF beta Receptor II aa 23-280. The exact sequence is proprietary.
Database link: P37173
- WB: HT-29 and A-549 cell lysates, mouse lung, spleen, brain and kidney tissues, rat lung tissue lysates; IHC: human breast cancer and human appendix; IF: NIH/3T3 cells.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.30
Preservative: 0.02% Sodium azide
Constituents: 49% PBS, 50% Glycerol
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab186838 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||1/50 - 1/200.|
|WB||1/500 - 1/2000. Predicted molecular weight: 65 kDa.|
|IHC-P||1/50 - 1/200.
ab171870 - Rabbit polyclonal IgG, is suitable for use as an isotype control with this antibody.
FunctionTransmembrane 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 is thus regulating 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 the activation of TGFRB1 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.
Involvement in diseaseDefects in TGFBR2 are the cause of hereditary non-polyposis colorectal cancer type 6 (HNPCC6) [MIM:614331]. Mutations in more than one gene locus can be involved alone or in combination in the production of the HNPCC phenotype (also called Lynch syndrome). Most families with clinically recognized HNPCC have mutations in either MLH1 or MSH2 genes. HNPCC is an autosomal, dominantly inherited disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early onset colorectal carcinoma (CRC) and extra-colonic cancers 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, and accounts for 15% of all colon cancers. Cancers in HNPCC originate within benign neoplastic polyps termed adenomas. Clinically, HNPCC is often divided into two subgroups. Type I: hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II: patients have an 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. HNPCC6 is a type of colorectal cancer complying with the clinical criteria of HNPCC, except that the onset of cancer was beyond 50 years of age in all cases.
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.
Sequence similaritiesBelongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. TGFB receptor subfamily.
Contains 1 protein kinase domain.
modificationsPhosphorylated on a Ser/Thr residue in the cytoplasmic domain.
Cellular localizationCell membrane.
- Information by UniProt
- AAT3 antibody
- FAA3 antibody
- LDS1B antibody
Paraffin-embedded human breast cancer tissue stained for TGF beta Receptor II using ab186838 at 1/100 dilution in immunohistochemical analysis.
Immunofluorescence staining of NIH/3T3 cells stained for TGF beta Receptor II with ab186838 at 1/100 dilution. Nuclei are labeled with DAPI (Blue).
All lanes : Anti-TGF beta Receptor II antibody (ab186838) at 1/1000 dilution
Lane 1 : HT-29 cell lysate
Lane 2 : A-549 cell lysate
Lane 3 : Mouse lung tissue lysate
Lane 4 : Mouse spleen tissue lysate
Lane 5 : Mouse brain tissue lysate
Lane 6 : Mouse kidney tissue lysate
Lane 7 : Rat lung tissue lysate
Lysates/proteins at 25 µg per lane.
All lanes : HRP Goat Anti-Rabbit IgG (H+L)
Developed using the ECL technique.
Predicted band size: 65 kDa
Exposure time: 3 seconds
Blocking buffer: 3% nonfat dry milk in TBST.
Paraffin-embedded human appendix tissue stained for TGF beta Receptor II using ab186838 at 1/100 dilution in immunohistochemical analysis.
ab186838 has been referenced in 34 publications.
- Nakamura Y et al. A disintegrin and metalloproteinase 12 prevents heart failure by regulating cardiac hypertrophy and fibrosis. Am J Physiol Heart Circ Physiol 318:H238-H251 (2020). PubMed: 31774689
- Fu X et al. miR-20a-5p/TGFBR2 Axis Affects Pro-inflammatory Macrophages and Aggravates Liver Fibrosis. Front Oncol 10:107 (2020). PubMed: 32117757
- Chen W et al. Kangquan Recipe Regulates the Expression of BAMBI Protein via the TGF-ß/Smad Signaling Pathway to Inhibit Benign Prostatic Hyperplasia in Rats. Evid Based Complement Alternat Med 2019:6281819 (2019). PubMed: 31186664
- Deng Z et al. lncRNA ATXN8OS promotes breast cancer by sequestering miR-204. Mol Med Rep 20:1057-1064 (2019). PubMed: 31173245
- Yin Z et al. Macrophage-derived exosomal microRNA-501-3p promotes progression of pancreatic ductal adenocarcinoma through the TGFBR3-mediated TGF-ß signaling pathway. J Exp Clin Cancer Res 38:310 (2019). PubMed: 31307515