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Activin A receptor, type IB

This gene encodes an activin A type IB receptor. 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 at least two type I and two type II receptors. This protein is a type I receptor which is essential for signaling. Mutations in this gene are associated with pituitary tumors. Alternate splicing results in multiple transcript variants.[provided by RefSeq, Jun 2010] (from NCBI)
Top mentioned proteins: SFRP1, TGF-beta, Smad2, ALK, TGF-beta type I receptor
Papers using ALK4 antibodies
Cis-regulatory inputs of the wnt8 gene in the sea urchin endomesoderm network
Patel Nipam, In PLoS Biology, 2004
... A stock solution of the ALK4/5/7 inhibitor SB-431542 (Tocris Biosciences) in dimethylsulfoxide was ...
Papers on ALK4
The TGF-β pathway mediates doxorubicin effects on cardiac endothelial cells.
Konorev et al., Hilo, United States. In J Mol Cell Cardiol, Jan 2016
Elevated ALK4/5 ligands including TGF-β and activins have been linked to cardiovascular remodeling and heart failure.
Uterine Activin-Like Kinase 4 Regulates Trophoblast Development During Mouse Placentation.
Matzuk et al., New York City, United States. In Mol Endocrinol, Dec 2015
Nodal, a TGF-β superfamily ligand, is essential for mesendoderm formation and left-right axis patterning during embryogenesis, and Nodal null mutants exhibit abnormal placental organization with expansion of trophoblast giant cells and a decrease of spongiotrophoblast and labyrinth.
ProNodal acts via FGFR3 to govern duration of Shh expression in the prechordal mesoderm.
Placzek et al., Lausanne, Switzerland. In Development, Dec 2015
Exposure of prechordal mesoderm microcultures to Nodal-conditioned medium, the Nodal inhibitor CerS, or to an ALK4/5/7 inhibitor reveals that Nodal is required to maintain both Shh and Gsc expression, but whereas Gsc is largely maintained through canonical signalling, Nodal signals through a non-canonical route to maintain Shh.
Transforming growth factor-β signaling induced during prostate cancer cell death and neuroendocrine differentiation is mediated by bone marrow stromal cells.
Sikes et al., Los Angeles, United States. In Prostate, Nov 2015
SMAD phosphorylation or activity during apoptosis and neuroendocrine differentiation was investigated using immunofluorescence, Western blotting, and luciferase reporter assays, along with the ALK-4, -5, -7 kinase inhibitor, SB-431542.
New Anti-Nodal Monoclonal Antibodies Targeting the Nodal Pre-Helix Loop Involved in Cripto-1 Binding.
Sandomenico et al., Napoli, Italy. In Int J Mol Sci, 2014
Typically, it also binds to the ALK4/ActRIIB receptor complex in the presence of the co-receptor Cripto-1.
PTP1B is an effector of activin signaling and regulates neural specification of embryonic stem cells.
Sun et al., Brno, Czech Republic. In Cell Stem Cell, 2014
We found that the Activin/ALK4 pathway directly recruits PTP1B and stimulates its release from the endoplasmic reticulum through ALK4-mediated cleavage.
Activin receptor antagonists for cancer-related anemia and bone disease.
Terpos et al., North Bay Shore, United States. In Expert Opin Investig Drugs, 2013
Antitumor activity has been observed preclinically with small-molecule inhibitors of transforming growth factor-β receptor type I (ALK5) that also antagonize the closely related activin receptors ALK4 and ALK7.
Activin receptor signaling: a potential therapeutic target for osteoporosis.
Baron et al., Boston, United States. In Curr Mol Pharmacol, 2012
The binding of activins to activin type IIA (ActRIIA) or type IIB (ActRIIB) receptors induces the recruitment and phosphorylation of an activin type I receptor (ALK4 and/or ALK7), which then phosphorylates the Smad2 and Smad3 intracellular signaling proteins.
Cell-type specific regulation of myostatin signaling.
Hoogaars et al., Leiden, Netherlands. In Faseb J, 2012
Results identify a molecular mechanism that explains the cell-type specific aspects of signaling by myostatin, ALK4, ALK5, and other TGF-beta family members.
Inhibin α-subunit N terminus interacts with activin type IB receptor to disrupt activin signaling.
Woodruff et al., Chicago, United States. In J Biol Chem, 2012
Inhibin alpha-subunit N terminus interacts with activin type IB receptor to disrupt activin signaling.
Nodal/Activin signaling drives self-renewal and tumorigenicity of pancreatic cancer stem cells and provides a target for combined drug therapy.
Heeschen et al., Madrid, Spain. In Cell Stem Cell, 2011
Knockdown or pharmacological inhibition of the Nodal/Activin receptor Alk4/7 in cancer stem cells virtually abrogated their self-renewal capacity and in vivo tumorigenicity
Conditional activin receptor type 1B (Acvr1b) knockout mice reveal hair loss abnormality.
Su et al., New York City, United States. In J Invest Dermatol, 2011
Our analysis of this Acvr1b knockout mouse line provides direct genetic evidence that Acvr1b signaling is required for both hair follicle development and cycling.
Activation of the activin A-ALK-Smad pathway in systemic sclerosis.
Yamanaka et al., Tokyo, Japan. In J Autoimmun, 2011
Activin A-ACVRIB/ALK4-Smad-dependent collagen production was augmented in SSc fibroblasts, suggesting the involvement of this signaling mechanism in systemic sclerosis.
Activin receptor-like kinase and the insulin gene.
Watanabe, Kyoto, Japan. In Vitam Horm, 2010
Activins signaling, which is mediated by ALK4 and 7 together with ActRIIA and IIB, plays a critical role in glucose-stimulated insulin secretion, development/neogenesis, and glucose homeostatic control of pancreatic endocrine cells; the insulin gene is regulated by these signaling pathways via ALK7, which is a receptor for Activins AB and B and Nodal.
Signal transduction pathway through activin receptors as a therapeutic target of musculoskeletal diseases and cancer.
Cui et al., Japan. In Endocr J, 2008
In the case of activins and nodal, activin receptor-like kinases 4 and 7 (ALK4 and ALK7) are the authentic type I receptors.
Reverse MAPPIT: screening for protein-protein interaction modifiers in mammalian cells.
Tavernier et al., Gent, Belgium. In Nat Methods, 2005
These reverse mammalian protein-protein interaction trap (MAPPIT) screens were developed to monitor interactions between the erythropoietin receptor (EpoR) and suppressors of cytokine signaling (SOCS) proteins, between FKBP12 and ALK4, and between MDM2 and p53.
Modulation of activin and BMP signaling.
Vale et al., Los Angeles, United States. In Mol Cell Endocrinol, 2004
Here, we summarize recent advances in understanding the mode of action of activins and BMPs, focusing on our elucidation of the crystal structure of BMP-7 in complex with the extracellular domain (ECD) of the activin type II receptor and our identification of a binding site for activin on the type I receptor ALK4.
Zebrafish Dpr2 inhibits mesoderm induction by promoting degradation of nodal receptors.
Meng et al., Beijing, China. In Science, 2004
Dpr2 binds to the TGFbeta receptors ALK5 and ALK4, and accelerates lysosomal degradation of these receptors
Betaglycan binds inhibin and can mediate functional antagonism of activin signalling.
Vale et al., Los Angeles, United States. In Nature, 2000
Activins bind specific type II receptor serine kinases (ActRII or IIB) to promote the recruitment and phosphorylation of the type I receptor serine kinase, ALK4 (refs 7-9), which then regulates gene expression by activating Smad proteins.
The EGF-CFC protein one-eyed pinhead is essential for nodal signaling.
Schier et al., New York City, United States. In Cell, 1999
Here we report that embryos lacking both maternal and zygotic Oep activity are defective in germ layer formation, organizer development, and the positioning of the anterior-posterior axis.
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