Transforming growth factor-β (TGF-β) family, including TGF-β, activin, Nodal, bone morphogenetic proteins (BMPs) and others, play vital roles in diverse cellular processes, including cell proliferation, differentiation, apoptosis, cell plasticity and migration. The type I receptor serine/threonine kinases (RSTKs) are also known as activin receptor-like kinases (ALKs) for which a systematic nomenclature has been proposed (ALK1-7) Its dysfunctions can result in various kinds of diseases, such as cancer and tissue fibrosis. Ligand binding leads to formation of the receptor heterocomplex, in which TGF-βRII phosphorylates threonine and serine residues of TGF-βRI and thus activates TGF-βRI. The activated TGF-βRI recruits and phosphorylates a subset of SMAD proteins (SMAD 2/3) which are then translocated to the nucleus where they form transcription complexes with DNA binding factors and co-activators/co-repressors to regulate transcription of the target genes. In normal cells, TGF-β, acting through its signaling pathway, stops the cell cycle at the G1 stage to stop proliferation, induce differentiation, or promote apoptosis. When a cell is transformed into a cancer cell, parts of the TGF-β signaling pathway are mutated, and TGF-β no longer controls the cell. These cancer cells proliferate.
Activins are dimeric growth and differentiation factors which belong to the transforming growth factor-beta (TGF-beta) superfamily of structurally related signaling proteins. Activins signal through a heteromeric complex of receptor serine kinases which include type I and type II receptors, and transduce signals through Smad-dependent and independent mechanisms. Type I receptors are essential for signaling; and type II receptors are required for binding ligands and for expression of type I receptors. Type I and II receptors form a stable complex after ligand binding, resulting in phosphorylation of type I receptors by type II receptors. Type II receptors are considered to be constitutively active kinases,.
 Regulation of TGF-β receptor activity. F. Huang Y.G. Chen. Cell Biosc. 2012, 2-9.
 Mechanisms of TGF-beta signaling from cell membrane to the nucleus. Shi Y, Massagué J. Cell. 2003, 113, 685-700.
 Activin receptor signaling: a potential therapeutic target for osteoporosis. S. Lotinun, R.S.Pearsall, W.C. Horne, R. Baron Curr. Mol. Pharmacol. 2012, 5, 195-204.
 Activin receptor antagonists for cancer-related anemia and bone disease. S.Z. Fields et al. Exp. Opinion Invest. Drugs 2013, 22, 87-101.
Items 1 to 15 of 20 total
|Axon ID||Name||Description||From price|
|1744||A 77-01||TGF-βR 1 inhibitor; ALK 5 inhibitor||€80.00|
|1421||A 83-01||TGF-βR 1 inhibitor; ALK 5 inhibitor||€75.00|
|1708||Dorsomorphin||Inhibitor of BMP signaling. Inhibits ALK2, 3 and 6||€65.00|
|2150||Dorsomorphin dihydrochloride||Inhibitor of BMP signaling. Inhibits ALK2, 3 and 6||€65.00|
|1832||GW 788388||TGF-βR 1 inhibitor||€60.00|
|2236||IN 1130||TGF-βR 1 inhibitor||€125.00|
|2323||ITD 1||Selective inhibitor of TGFβ/Smad signaling that promotes cardiogenesis||€105.00|
|2467||ITD-1, (+)-||Selective inhibitor of TGFβ/Smad signaling that promotes cardiogenesis||€165.00|
|2189||K 02288||Inhibitor of BMP signaling. Inhibits ALK1, 2, and 6||€90.00|
|1509||LDN 193189 hydrochloride||Highly potent small molecule inhibitor of BMP type I receptors ALK2, ALK3, and ALK6||€70.00|
|2201||LDN 212854 trihydrochloride||Potent ALK2-biased BMP type I receptor kinase inhibitor||€105.00|
|1491||LY 2157299||TGF-βR2 inhibitor||€70.00|
|1661||SB 431542||TGF-βR1 inhibitor; ALK inhibitor||€70.00|
|2197||SB 505124||Selective inhibitor of TGF-β type I receptors ALK4 and ALK5||€95.00|
|2285||SB 525334||Potent and selective inhibitor of the TGF-βR1 (ALK5) receptor||€105.00|