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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Small Molecule to Inhibit ALK5 for Alopecia and Fibrosis - Drug Profile 129 Fibrosis - Recent Pipeline Updates 130 Fibrosis - Dormant Projects 147 Fibrosis - Product Development Milestones 148 Featured News & Press Releases 148 Appendix 155 Methodology 155 Coverage 155 Secondary Research 155 Primary Research 155 Expert Panel Validation 155 Contact Us 156 Disclaimer 156 List of Tables Number of Products under Development for Fibrosis, H1 2014 13 Number of Products under Development for Fibrosis - Comparative Analysis, H1 2014 14 Number of Products under Development by Companies, H1 2014 16 Number of Products under Development by Companies, H1 2014 (Contd.
Fibrosis - Pipeline Review, H1 2014
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
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.
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
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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