TGFBR1

(redirected from ALK5)

TGFBR1

A gene on chromosome 9q22 that encodes a transmembrane kinase of the TGFB receptor subfamily of Ser/Thr protein kinases, which forms a heteromer with type-II TGF-beta receptors and binds TGF-beta. This receptor/ligand complex phosphorylates proteins which enter the nucleus and regulate transcription of cell proliferation-related genes.

Molecular pathology
TGFBR1 mutations are associated with Loeys-Deitz aortic aneurysm syndrome.
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Krystof, ALK5 kinase inhibitory activity and synthesis of 2,3,4-substituted 5,5-dimethyl-5,6-dihydro-4H-pyrrolo[1,2-b]pyra zoles.
Synthesis and Insecticidal, Anticancer Activity of Novel Pyrazole Acyl Urea Derivatives
Similarly, the effect of TPT on resistant MCF-7 cells was also increased either by ALK5 (TGF[beta]RI) siRNA or by a small molecular inhibitor of ALK5, SB-431542.
On-Target plus siRNAs targeting human ALK5 (L-003929-000005) and snail (L-010847-01-0005) were purchased from Dharmacon (Lafayette, CO) and transfected using Dharmafect Duo transfection reagents, following the manufacturer's instructions.
The expression of ALK5, E-cadherin and vimentin within MDAMB-231 xenografts were detected by immunohistochemical techniques.
MHP-1 inhibits cancer metastasis and restores topotecan sensitivity via regulating epithelial-mesenchymal transition and TGF-[beta] signaling in human breast cancer cells
2011); while the GDF9 uses a signaling pathway via activin-TGF-[beta], binding to its BMPRII and ALK5 receptors and subsequently activating the Smads 2 and 3 (Vitt et al.
Role of growth differentiation factor 9 and bone morphogenetic protein 15 in ovarian function and their importance in mammalian female fertility--a review
Epithelial and ectomesenchymal role of the type I TGF- receptor ALK5 during facial morphogenesis and palatal fusion.
Bases geneticas de la formacion de fisuras labiales y/o palatinas en humanos
Using a mouse model of cancer, they show that blocking the action of a signalling molecule called ALK5 makes tumour blood vessels even leakier for a short period of time, and this window of leakiness can be used to "open up" the tumour for more efficient delivery of drugs.
Blocking the ALK5 pathway may not only make chemotherapy far more effective in multiple cancers, but could also aid in efficient delivery of the many other therapies that rely on the bloodstream to carry them into a tumour.
Further, ALK5 blockade could assist in diagnosis as well as treatment; the imaging molecules used to light up tumours so that they can be seen by scanners might also be able to get in more easily if ALK5 were inactivated at the time of scanning.
Exploiting cancers' own architecture may lead to their destruction
According to reports in this field (25, 30, 31, 36), TGF-[beta] can signal through two type I receptors, ALK1 and ALK5, which display different affinities for TGF-[beta1].
Mutation analysis in Spanish patients with hereditary hemorrhagic telangiectasia: deficient endoglin up-regulation in activated monocytes
Transforming growth factor-beta1 causes pulmonary microvascular endothelial cell apoptosis via ALK5 (Lu et al.
The signaling mechanism of TGF-[[beta].sub.1] induced bovine mammary epithelial cell apoptosis
Moreover, there have been few reports on the influence of expression of BMPRII, BMPRIB and ALK5 by daidzein in ovine granulosa cells.
Effects of daidzein on mRNA expression of bone morphogenetic protein receptor type I and II genes in the ovine granulosa cells

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