ACVR1B

(redirected from ALK4)

ACVR1B

A gene on chromosome 12q13 that encodes activin receptor type IB, a receptor that forms a complex with other type-I and two type-II  transmembrane serine/threonine kinase receptors for activin, a dimeric growth and differentiating factor belonging to the TGF-beta superfamily of structurally related signalling proteins. Type-II receptors phosphorylate and activate type-I receptors, which autophosphorylate, then bind and activate SMAD transcriptional regulators, playing roles in cell differentiation, growth arrest and apoptosis. 

Molecular pathology
ACVR1B mutations are associated with pituitary tumours.
References in periodicals archive ?
SB-431542 is a potent and specific inhibitor of transforming growth factor-beta superfamily type I activin receptor-like kinase (ALK) receptors ALK4, ALK5, and ALK7.
SB431542 is a selective and potent inhibitor of the TGF-[beta] pathway through suppression of the activin A receptors ALK5, ALK4, and ALK7.
Callahan et al., "SB-431542 is a potent and specific inhibitor of transforming growth factor-beta superfamily type I activin receptor-like kinase (ALK) receptors ALK4, ALK5, and ALK7," Molecular Pharmacology, vol.
Callahan et al., "SB-431542 is a potent and specific inhibitor of transforming growth factor-[beta] superfamily type I activin receptor-like kinase (ALK) receptors ALK4, ALK5, and ALK7," Molecular Pharmacology, vol.
Vale, "Identification of a functional binding site for activin on the type I receptor ALK4," Journal of Biological Chemistry, vol.
Activin and MSTN association with ActRIIB leads to the recruitment, phosphorylation, and activation of the activin type I receptor, activin receptor-like kinase 4 (ALK4).
miR-221, miR-222, and miR-24 inhibit normal erythropoiesis and miR-24 targets ALK4. cMyb and miR-15a are involved in the transition from BFU-E to CFU-E stage [61-63].
ACVR1B (ALK4, activin receptor type 1B) gene mutations in pancreatic carcinoma.
SB431542 blocks SMAD2/3 phosphorylation and nuclear translocation by inhibiting the activation of the transforming growth factor-beta superfamily type I activin receptor-like kinase (ALK) receptors ALK4, ALK5, and ALK7 [34].
Treatment with SB431542, an inhibitor of Alk4, 5, and 7, PDGF, bFGF, oncostatin, and IGF was able to induce these Pax3(+) myogenic precursor cells into around 50-60% of MyoD(+) myoblasts in an additional 8 days.
ActA binds to type II receptor, ACVR2A or ACVR2B, leading to oligomerization, which recruits and phosphorylates the activin type I receptor-like kinase 4 (ALK4, or also known as ACVR1B) (reviewed in [26]).
The specific inhibition of the activin and nodal receptors, Alk4 and Alk7, and the TGF[beta] receptor, Alk5, avoids Smad2/Smad3 phosphorylation and the subsequent initiation of downstream signalling [90].