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Mouse (Murine) Polyclonal ACVR1C Primary Antibody für WB - ABIN658527
Andersson, Korach-Andre, Reissmann, Ibáñez, Bertolino: Growth/differentiation factor 3 signals through ALK7 and regulates accumulation of adipose tissue and diet-induced obesity. in Proceedings of the National Academy of Sciences of the United States of America 2008
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Human Polyclonal ACVR1C Primary Antibody für IHC (p), WB - ABIN391157
Munir, Xu, Wu, Yang, Lala, Peng: Nodal and ALK7 inhibit proliferation and induce apoptosis in human trophoblast cells. in The Journal of biological chemistry 2004
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Loss of ALK7 expression are associated with invasion, metastasis of the pancreatic ductal adenocarcinoma.
Alk7 is expressed in male germ cells and Sertoli cells.
ACVR (zeige ACRV1 Antikörper) 1C is a tumor suppressor, and lowered ACVR (zeige ACRV1 Antikörper) 1C expression is an important marker for the metastasis, invasion, and prognosis of gallbladder cancer.
Our findings suggested that the ALK7 gene polymorphism rs13010956 was significantly associated with metabolic syndrome risk in females and may be involved in cardiovascular remodeling in metabolic syndrome patients.
reduction or lack of ALK7 expression may account for the loss of its ligand sensitivity of breast cancer cells, thereby leading to breast tumor progression.
These findings suggest that the Nodal/ALK7 pathway plays important roles in human placentation and that its abnormal signaling may contribute to the development of preeclampsia.
ALK7 and its isoforms are expressed in human placentae of different stages of pregnancy and that their expression is developmentally regulated
ALK7 induces apoptosis through activation of the traditional TGF-beta (zeige TGFB1 Antikörper) pathway components
the Nodal-ALK7 pathway inhibits cell proliferation by inducing G(1) cell cycle arrest
AB and activin B and is responsible for ac (zeige Actbeta Antikörper)tivin-mediated se (zeige Actbeta Antikörper)cretion of insulin from pancrea (zeige Actbeta Antikörper)tic beta cell line, MIN6.
Data, including data from studies using knockout mice, suggest that Gdf3 (zeige GDF3 Antikörper)-Alk7 axis between adipose tissue macrophages and adipocytes represents previously unrecognized mechanism by which insulin (zeige INS Antikörper) regulates both fat metabolism/lipolysis and adiposity. (Gdf3 (zeige GDF3 Antikörper) = growth differentiation factor-3 (zeige GDF3 Antikörper); Alk7 = activin receptor-like kinase-7)
Thus, the authors define a new memory mechanism by which learning reverses microRNA-mediated silencing of the novel plasticity protein ACVR1C via translin (zeige TSN Antikörper)/trax (zeige TSNAX Antikörper).
ALK7 protects against pathological cardiac hypertrophy in mice.
These findings suggest that endogenous expression of ALK7 is necessary to maintain repolarizing K+ currents in ventricular cardiomyocytes, and finally prevent action potential prolongation and ventricular arrhythmia.
ALK7 signaling contributes to diet-induced catecholamine resistance in adipose tissue; ALK7 inhibitors may have therapeutic value in human obesity.
Signaling through the TGF beta (zeige TGFB1 Antikörper)-activin (zeige Actbeta Antikörper) receptors ALK4 (zeige ACVR1B Antikörper)/5/7 regulates testis formation and male germ cell development.
Alk7 is involved in modulation of adipose tissue metabolism in response to beta3-adrenergic receptor (zeige ADRB3 Antikörper) activation.
Data indicate that activin receptor ALK7-knockout females showed delayed onset of puberty and abnormal estrous cyclicity.
Activin receptor-like kinase 7 suppresses lipolysis to accumulate fat in obesity through downregulation of peroxisome proliferator-activated receptor gamma (zeige PPARG Antikörper) and C/EBPalpha (zeige CEBPA Antikörper).
Knockdown or pharmacological inhibition of the Nodal/Activin receptor Alk4 (zeige ACVR1B Antikörper)/7 in cancer stem cells virtually abrogated their self-renewal capacity and in vivo tumorigenicity
ACVR1C is a type I receptor for the TGFB (see MIM 190180) family of signaling molecules. Upon ligand binding, type I receptors phosphorylate cytoplasmic SMAD transcription factors, which then translocate to the nucleus and interact directly with DNA or in complex with other transcription factors (Bondestam et al., 2001
, activin receptor type IC
, activin receptor type-1C
, activin receptor-like kinase 7
, TGF-beta type 1 receptor
, activin A receptor, type IC