Key features and details
- Mouse monoclonal [MM0056-4F14] to TGF beta Receptor II
- Suitable for: IHC-Fr, Flow Cyt, IHC-P
- Reacts with: Human
- Isotype: IgG1
Product nameAnti-TGF beta Receptor II antibody [MM0056-4F14]
See all TGF beta Receptor II primary antibodies
DescriptionMouse monoclonal [MM0056-4F14] to TGF beta Receptor II
Specificityab78419 detects TGF beta Receptor II. No cross reactivity was found to rTGF beta Receptor III.
Tested applicationsSuitable for: IHC-Fr, Flow Cyt, IHC-Pmore details
Species reactivityReacts with: Human
Recombinant human TGF beta Receptor II extracellular domain
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Storage bufferConstituent: PBS
Concentration information loading...
PurityProtein G purified
Purification notesThe IgG fraction of culture supernatant was purified by Protein G affinity chromatography and lyophilized from a 0.2 µm filtered solution in phosphate buffered saline (PBS).
Our Abpromise guarantee covers the use of ab78419 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-Fr||Use at an assay dependent concentration.|
|Flow Cyt||Use 1µg for 106 cells.
ab170190 - Mouse monoclonal IgG1, is suitable for use as an isotype control with this antibody.
|IHC-P||1/50 - 1/200.|
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
ab78419 at 1/200 dilution, staining TGF beta Receptor II in human placental tissue section by Immunohistochemistry (Formalin/PFA fixed paraffin-embedded sections).
Overlay histogram showing HepG2 cells stained with ab78419 (red line). The cells were fixed with 80% methanol (5 min) and incubated in 1x PBS / 10% normal goat serum / 0.3M glycine to block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab78419, 1µg/1x106 cells) for 30 min at 22ºC. The secondary antibody used was DyLight® 488 goat anti-mouse IgG (H+L) (ab96879) at 1/500 dilution for 30 min at 22ºC. Isotype control antibody (black line) was mouse IgG1 [ICIGG1] (ab91353, 2µg/1x106 cells) used under the same conditions. Acquisition of >5,000 events was performed.
Please note that Abcam do not have any data for use of this antibody on non-fixed cells. We welcome any customer feedback.
Immunohistochemical analysis of Human lung frozen tissue sections (A - alveolar macrophages, B - lung carcinoma), labeling TGF beta Receptor II with ab78419. Samples were fixed in HOPE and immunostained with ab78419 diluted 1/400 for 1 hour at 25°C.
ab78419 has been referenced in 17 publications.
- Gu Y et al. Integrated network analysis identifies hsa-miR-4756-3p as a regulator of FOXM1 in Triple Negative Breast Cancer. Sci Rep 9:13830 (2019). PubMed: 31554904
- Jiang Y et al. Discovery of microarray-identified genes associated with the progression of cervical intraepithelial neoplasia. Int J Clin Exp Pathol 11:5667-5681 (2018). PubMed: 31949653
- Song K et al. ERBB3, IGF1R, and TGFBR2 expression correlate with PDGFR expression in glioblastoma and participate in PDGFR inhibitor resistance of glioblastoma cells. Am J Cancer Res 8:792-809 (2018). PubMed: 29888103
- Breunig C et al. TGFß1 regulates HGF-induced cell migration and hepatocyte growth factor receptor MET expression via C-ets-1 and miR-128-3p in basal-like breast cancer. Mol Oncol 12:1447-1463 (2018). Flow Cyt ; Human . PubMed: 30004628
- Fan Y et al. YAP-1 Promotes Tregs Differentiation in Hepatocellular Carcinoma by Enhancing TGFBR2 Transcription. Cell Physiol Biochem 41:1189-1198 (2017). PubMed: 28472799