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Activins are dimeric growth and differentiation factors which belong to the transforming growth factor-beta (TGF-beta) superfamily of structurally related signaling proteins. 再加上，我们可以发Activin Receptor Type I 蛋白 (35) 和 Activin Receptor Type I 试剂盒 (16)和数多这个蛋白质的别的产品。
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Human Polyclonal ACRV1 Primary Antibody for CyTOF, FACS - ABIN4899715
Fujimoto, Ohte, Shin, Yoneyama, Osawa, Miyamoto, Tsukamoto, Mizuta, Kokabu, Machiya, Okuda, Suda, Katagiri: Establishment of a novel model of chondrogenesis using murine embryonic stem cells carrying fibrodysplasia ossificans progressiva-associated mutant ALK2. in Biochemical and biophysical research communications 2014
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Human Polyclonal ACRV1 Primary Antibody for IHC (p), WB - ABIN392240
ten Dijke, Ichijo, Franzén, Schulz, Saras, Toyoshima, Heldin, Miyazono: Activin receptor-like kinases: a novel subclass of cell-surface receptors with predicted serine/threonine kinase activity. in Oncogene 1993
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Human Polyclonal ACRV1 Primary Antibody for IHC (p), IHC - ABIN256737
Shore, Xu, Feldman, Fenstermacher, Cho, Choi, Connor, Delai, Glaser, LeMerrer, Morhart, Rogers, Smith, Triffitt, Urtizberea, Zasloff, Brown, Kaplan: A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva. in Nature genetics 2006
Acute tacrolimus treatment transiently increases hepcidin (显示 HAMP 抗体) in wild-type mice. FKBP12 (显示 FKBP1A 抗体) preferentially targets the BMP receptor (显示 BMPR1A 抗体) ALK2. ALK2 mutants defective in binding FKBP12 (显示 FKBP1A 抗体) increase hepcidin (显示 HAMP 抗体) expression in a ligand-independent manner, through BMP-SMAD (显示 SMAD1 抗体) signaling.
The authors demonstrated that ubiquitin-specific protease (USP) 4 (显示 USP4 抗体) strongly induces activin (显示 Actbeta 抗体)/BMP signaling by removing the inhibitory monoubiquitination from SMAD4 (显示 SMAD4 抗体).
Enhanced SMAD (显示 SMAD1 抗体)-dependent BMP signaling through constitutively active ACVR1 in palatal epithelium causes submucous cleft palate in mice, via medial-edge-epithelium persistence presumably due to the up regulation of DeltaNp63 andresultingreductionofcaspase-3 activation. 2.
BMP signaling mediated by coordination of ALK2/ACVR1, ALK3/BMPR1A (显示 BMPR1A 抗体), and BMPR2 (显示 BMPR2 抗体) is an essential proangiogenic cue for retinal vessels.
This study showed that Gja1 (显示 GJA1 抗体) may act downstream of cAMP-PKA signal to mediate the effects of Acvr1 on the differentiation of uterine stromal cells through targeting Hand2 (显示 HAND2 抗体).
Results showed activin (显示 Actbeta 抗体)-C and follistatin (显示 FST 抗体) are differentially expressed during prostate development and suggested that the antagonistic property of follistatin (显示 FST 抗体) is secondary to the action of activin (显示 Actbeta 抗体)-C. Study provides evidence to support a role of activin (显示 Actbeta 抗体)-C in prostate development and provides new insights in the spatiotemporal localization of activins and their antagonists during mouse prostate development.
BMPR1B plays distinct roles from BMPR1A and ACVR1 in maintaining bone mass and transducing BMP signaling
Suggest that BMP signaling upregulates the calcineurin/nuclear factor of activated T cell (显示 NFATC3 抗体) pathway via BMP type I receptor ALK2, contributing to cardiac hypertrophy and fibrosis.
results suggest that ACVR1(R206H) causes FOP (显示 CHTOP 抗体) by gaining responsiveness to the normally antagonistic ligand activin A (显示 INHBA 抗体), demonstrating that this ligand is necessary and sufficient for driving HO in a genetically accurate model of FOP (显示 CHTOP 抗体)
The findings suggest that the mutant ALK2 related to Fibrodysplasia ossificans progressiva is enhanced by bone morphogenetic protein type II receptors via the T203-regulated phosphorylation of ALK2.
the Fibrodysplasia Ossificans Progressiva mutation ACVR1(R206H) is more sensitive to a number of natural ligands.
both bone morphogenetic protein 2 (BMP2 (显示 BMP2 抗体)) and BMP6 (显示 BMP6 抗体) are proangiogenic in vitro and ex vivo and that the BMP type I receptors, activin receptor-like kinase 3 (ALK3 (显示 BMPR1A 抗体)) and ALK2, play crucial and distinct roles in this process.
Fibrodysplasia ossificans progressiva (FOP) syndrome is caused by mutation of the gene ACVR1. Developed is a simplified one-step procedure by simultaneously introducing reprogramming and gene-editing components into human fibroblasts derived from patient with FOP. The one-step-mediated ALK2 gene-corrected induced pluripotent stem cells restored global gene expression pattern.
The ACVR1 R206H mutation may not directly increase the formation of mature chondrogenic or osteogenic cells.
Authors demonstrated that the BMP type I receptor ALK-2 (encoded by the ACVR1 gene) has crucial roles in apoptosis induction of patient-derived glioma-initiating cells (GICs), TGS (显示 LIN9 抗体)-01 and TGS (显示 LIN9 抗体)-04.
Data suggest BMP9/GDF2 (显示 GDF2 抗体) and BMP10 (显示 BMP10 抗体) synergize with TNFA (显示 TNF 抗体) to increase monocyte recruitment to vascular endothelial cells; process appears to be mediated mainly via ALK2/ACVR1 (which exhibits protein kinase (显示 CDK7 抗体) activity). These studies used in vitro flow monocyte adhesion assay. (BMP9 (显示 GDF2 抗体) = growth differentiation factor 2 (显示 GDF2 抗体); BMP10 (显示 BMP10 抗体) = bone morphogenetic protein 10 (显示 BMP10 抗体); TNFA (显示 TNF 抗体) = tumor necrosis factor alpha (显示 TNF 抗体); ALK2/ACVR1 = activin A receptor type 1)
The effects of ACVR1/ALK2 mutations causing fibrodysplasia ossificans progressiva are extended to the central nervous system. Brainstem hamartomatous lesions and dysmorphisms, variably associated with dentate nucleus and basal ganglia signal abnormalities and/or calcifications, may represent useful disease hallmarks.
Low ALK2 expression is associated with invasiveness of breast cancer.
Further investigation on clinical ESCC samples and non-tumorous adjacent tissue found that tumors with triple-positive BMP6 (显示 BMP6 抗体), ALK2 and BMPRII (显示 BMPR2 抗体) had deeper growth than tumors with only BMP6 (显示 BMP6 抗体) expression
The clinical manifestations, the disease course, and the molecular findings of involvement of ACVR1 gene in this family are suggestive of "FOP variant" or an unusual ACVR1-related skeletal dysplasia
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 ( I and IB) and two type II (II and IIB) receptors. These receptors are all transmembrane proteins, composed of a ligand-binding extracellular domain with cysteine-rich region, a transmembrane domain, and a cytoplasmic domain with predicted serine/threonine specificity. 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. This gene encodes activin A type I receptor which signals a particular transcriptional response in concert with activin type II receptors. Mutations in this gene are associated with fibrodysplasia ossificans progressive.
TGF-B superfamily receptor type I
, activin receptor type I
, activin receptor type-1
, serine/threonine-protein kinase receptor R1
, activin A receptor, type II-like kinase 2
, activin receptor-like kinase 2
, hydroxyalkyl-protein kinase
, activin A receptor, type 1
, activin type I receptor
, type I TGF B receptor
, activin A receptor, type I
, activin receptor type IA