Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Rabbit monoclonal [EPR14673] to TGF beta Receptor II
- Suitable for: WB
- Knockout validated
- Reacts with: Human
Product nameAnti-TGF beta Receptor II antibody [EPR14673]
See all TGF beta Receptor II primary antibodies
DescriptionRabbit monoclonal [EPR14673] to TGF beta Receptor II
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Human
Recombinant fragment within Human TGF beta Receptor II aa 1-150. The exact sequence is proprietary.
Database link: P37173
- WB: HepG2 and A549 and HT-1080 cell lysates.
This product is a recombinant monoclonal antibody, which offers several advantages including:
- - High batch-to-batch consistency and reproducibility
- - Improved sensitivity and specificity
- - Long-term security of supply
- - Animal-free production
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
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 bufferPreservative: 0.01% Sodium azide
Constituents: 59% PBS, 40% Glycerol, 0.05% BSA
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab184948 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000 - 1/10000. Detects a band of approximately 70-80 kDa (predicted molecular weight: 65 kDa).|
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
All lanes : Anti-TGF beta Receptor II antibody [EPR14673] (ab184948) at 1/2000 dilution
Lane 1 : Wild-type A549 whole cell lysate at 40 µg
Lane 2 : TGFBR2 knockout A549 whole cell lysate at 40 µg
Lane 3 : HepG2 whole cell lysate at 20 µg
Lane 4 : HT-1080 whole cell lysate at 20 µg
Predicted band size: 65 kDa
Observed band size: 80 kDa why is the actual band size different from the predicted?
Lanes 1 - 4: Merged signal (red and green). Green - ab184948 observed at 80 kDa. Red - loading control, ab8245, observed at 37 kDa.
ab184948 was shown to specifically react with in wild-type A549 cells as signal was lost in TGFBR2 knockout cells. Wild-type and TGFBR2 knockout samples were subjected to SDS-PAGE. Ab184948 and ab8245 (Mouse anti-GAPDH loading control) were incubated overnight at 4°C at 1/2000 dilution and 1/10000 dilution respectively. Blots were developed with Goat anti-Rabbit IgG H&L (IRDye® 800CW) preabsorbed ab216773 and Goat anti-Mouse IgG H&L (IRDye® 680RD) preabsorbed ab216776 secondary antibodies at 1/10000 dilution for 1 hour at room temperature before imaging.
All lanes : Anti-TGF beta Receptor II antibody [EPR14673] (ab184948) at 1/5000 dilution
Lane 1 : HepG2 cell lysate
Lane 2 : A549 cell lysate
Lysates/proteins at 20 µg per lane.
All lanes : Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/1000 dilution
Predicted band size: 65 kDa
ab184948 has been referenced in 9 publications.
- Sasaki N et al. Rapamycin promotes endothelial-mesenchymal transition during stress-induced premature senescence through the activation of autophagy. Cell Commun Signal 18:43 (2020). PubMed: 32164764
- Liu D et al. Protein diaphanous homolog 1 (Diaph1) promotes myofibroblastic activation of hepatic stellate cells by regulating Rab5a activity and TGFß receptor endocytosis. FASEB J 34:7345-7359 (2020). PubMed: 32304339
- Chavez RD et al. Prg4 prevents osteoarthritis induced by dominant-negative interference of TGF-ß signaling in mice. PLoS One 14:e0210601 (2019). PubMed: 30629676
- He W et al. MSC-regulated lncRNA MACC1-AS1 promotes stemness and chemoresistance through fatty acid oxidation in gastric cancer. Oncogene 38:4637-4654 (2019). PubMed: 30742067
- Cao T et al. H19 lncRNA identified as a master regulator of genes that drive uterine leiomyomas. Oncogene 38:5356-5366 (2019). PubMed: 31089260
- Huang C et al. Berberine reversed the epithelial-mesenchymal transition of normal colonic epithelial cells induced by SW480 cells through regulating the important components in the TGF-ß pathway. J Cell Physiol N/A:N/A (2018). WB ; Human . PubMed: 30536375
- Ma F et al. MicroRNA-19a promotes nasopharyngeal carcinoma by targeting transforming growth factor ß receptor 2. Exp Ther Med 14:1419-1426 (2017). PubMed: 28810605
- Yang YH et al. Stromal Tissue Rigidity Promotes Mesenchymal Stem Cell-Mediated Corneal Wound Healing Through the Transforming Growth Factor ß Signaling Pathway. Stem Cells 34:2525-2535 (2016). PubMed: 27250866
- Yumoto K et al. Axl is required for TGF-ß2-induced dormancy of prostate cancer cells in the bone marrow. Sci Rep 6:36520 (2016). WB ; Human . PubMed: 27819283