alk5 Proteins, Antibodies, cDNA Clones Research Reagents

TGFBR1 (Transforming Growth Factor Beta Receptor 1) is a protein coding gene located on human chromosome 9q22.33. TGFBR1 is also known as AAT5, ALK5, ESS1, LDS1, MSSE, SKR4, TBRI, ALK-5, LDS1A, LDS2A, TBR-i, TGFR-1, ACVRLK4 and tbetaR-I. The human TGFBR1 gene encodes a 55960 Da protein containing 503 amino acids. The TGFBR1 protein is ubiquitously expressed in placenta, gall bladder and other tissues. Among its related pathways are Transcriptional activity of SMAD2/SMAD3-SMAD4 heterotrimer and Cell adhesion_Plasmin signaling. TGFBR1 is related to transferase activity, transferring phosphorus-containing groups and protein tyrosine kinase activity. ACVR1B is an important paralog of TGFBR1 gene. TGFBR1 is associated with some diseases, including Multiple Self-Healing Squamous Epithelioma and Loeys-Dietz Syndrome 1.

alk5 Protein (3)

    alk5 Antibody (1)

      alk5 cDNA Clone (39)

      NM_004612.2
      NM_009370.2
      XM_538750.3

      alk5 Lysate (3)

        alk5 Background

        Transforming growth factor, beta receptor I, also known as Transforming growth factor-beta receptor type I , Serine / threonine-protein kinase receptor R4, Activin receptor-like kinase 5, SKR4, ALK-5, and TGFBR1, is a single-pass type I membrane protein that belongs to the protein kinase superfamily and TGFB receptor subfamily. TGFBR1 / ALK-5 is found in all tissues examined. It is most abundant in placenta and least abundant in brain and heart. TGF-beta functions as a tumor suppressor by inhibiting the cell cycle in the G1 phase. Administration of TGF-beta is able to protect against mammary tumor development in transgenic mouse models in vivo. Disruption of the TGF-beta/SMAD pathway has been implicated in a variety of human cancers, with the majority of colon and gastric cancers being caused by an inactivating mutation of TGF-beta RII. On ligand binding, TGFBR1 / ALK-5 forms a receptor complex consisting of two type I I and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which auto-phosphorylate, then bind and activate SMAD transcriptional regulators. TGF-beta signaling via TGFBR1 / ALK-5 is not required in myocardial cells during mammalian cardiac development, but plays an irreplaceable cell-autonomous role regulating cellular communication, differentiation and proliferation in endocardial and epicardial cells. Defects in TGFBR1 / ALK-5 are the cause of Loeys-Dietz syndrome type 1A (LDS1A), Loeys-Dietz syndrome type 2A (LDS2A), and aortic aneurysm familial thoracic type 5 (AAT5).

        alk5 References

        • Seki T, et al. (2006) Nonoverlapping expression patterns of ALK1 and ALK5 reveal distinct roles of each receptor in vascular development. Lab Invest. 86(2): 116-29. et al.
        • Piek E, et al. (1999) TGF-(beta) type I receptor/ALK-5 and Smad proteins mediate epithelial to mesenchymal transdifferentiation in NMuMG breast epithelial cells. J Cell Sci. 112 (24): 4557-68. et al.
        • Dudas M, et al. (2004) Tgf-beta3-induced palatal fusion is mediated by Alk-5/Smad pathway. Dev Biol. 266(1): 96-108.

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