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Human Polyclonal ACVR1C Primary Antibody für IHC (p), ELISA - ABIN543603
Roberts, Hu, Qiu, Leung, Caniggia, Gruslin, Tsang, Peng: Identification of novel isoforms of activin receptor-like kinase 7 (ALK7) generated by alternative splicing and expression of ALK7 and its ligand, Nodal, in human placenta. in Biology of reproduction 2003
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Human Monoclonal ACVR1C Primary Antibody für CyTOF, FACS - ABIN4899939
Puvanenthiran, Essapen, Seddon, Modjtahedi et al.: Impact of the putative cancer stem cell markers and growth factor receptor expression on the sensitivity of ovarian cancer cells to treatment with various forms of small molecule tyrosine kinase ... in International journal of oncology 2017
Human Monoclonal ACVR1C Primary Antibody für FACS - ABIN4896938
Tengroth, Arebro, Larsson, Bachert, Georén, Cardell: Activation of Activin receptor-like kinases curbs mucosal inflammation and proliferation in chronic rhinosinusitis with nasal polyps. in Scientific reports 2018
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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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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MiR-454 binds to the 3'-UTR of ALK7 and regulates ALK7 expression in placenta.ALK7 signaling is regulated by MicroRNA-454 in the placental tissues from pre-eclampsia patients.
reduced expression in sensitive skin; plays crucial roles in the pathogenesis of sensitive skin
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 1C is a tumor suppressor, and lowered ACVR 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.
cDNA cloning, expression studies and chromosome mapping
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 pathway components
the Nodal-ALK7 pathway inhibits cell proliferation by inducing G(1) cell cycle arrest
AB and activin B and is responsible for activin-mediated secretion of insulin from pancreatic beta cell line, MIN6.
ALK7-induced apoptosis is at least in part through two Smad-dependent pathways, Bax/Bcl-2 and Xiap.
GDF3 regulates adipose-tissue homeostasis and energy balance under nutrient overload in part by signaling through the ALK7 receptor
The antiproliferative effect of Nodal/ALK7 on ovarian cancer cells is in part mediated by cyclin G2.
One of the direct target genes in the ALK7 signaling pathway is the insulin gene in pancreatic beta-cells, and that PDX-1 is directly involved in this pathway through interaction with Smad2 and Smad3.
Microarray analysis showed that adipose tissue expressed activin type I and II receptors and that the expression of activin receptor-like kinase 7 was adipose tissue specific.
Data, including data from studies using knockout mice, suggest that Gdf3-Alk7 axis between adipose tissue macrophages and adipocytes represents previously unrecognized mechanism by which insulin regulates both fat metabolism/lipolysis and adiposity. (Gdf3 = growth differentiation factor-3; 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/trax.
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-activin receptors ALK4/5/7 regulates testis formation and male germ cell development.
Alk7 is involved in modulation of adipose tissue metabolism in response to beta3-adrenergic receptor 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 and C/EBPalpha.
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
ALK7 is the signaling receptor for activin AB and activin B and is responsible for activin-mediated secretion of insulin from pancreatic beta cell line, MIN6.
ALK7 is not an essential mediator of Nodal signaling during mesendoderm formation and left-right patterning in the mouse but may instead mediate other activities of Nodal and related ligands in the development or function of particular tissues and organs
These results indicated that ALK7 is a novel marker specifically expressed during the late phase of adipocyte differentiation.
ALK7 plays an important role in regulating the functional plasticity of pancreatic islets, negatively affecting beta-cell function by mediating the effects of activin B on Ca(2+) signaling
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