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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. Additionally we are shipping Activin Receptor Type I Proteins (35) and Activin Receptor Type I Kits (15) and many more products for this protein.
Showing 10 out of 169 products:
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
Show all 4 Pubmed References
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
Show all 2 Pubmed References
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
The authors demonstrated that ubiquitin-specific protease (USP) 4 (show USP4 Antibodies) strongly induces activin (show Actbeta Antibodies)/BMP signaling by removing the inhibitory monoubiquitination from SMAD4 (show SMAD4 Antibodies).
Enhanced SMAD (show SMAD1 Antibodies)-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 (show BMPR1A Antibodies), and BMPR2 (show BMPR2 Antibodies) is an essential proangiogenic cue for retinal vessels.
This study showed that Gja1 (show GJA1 Antibodies) may act downstream of cAMP-PKA signal to mediate the effects of Acvr1 on the differentiation of uterine stromal cells through targeting Hand2 (show HAND2 Antibodies).
Results showed activin (show Actbeta Antibodies)-C and follistatin (show FST Antibodies) are differentially expressed during prostate development and suggested that the antagonistic property of follistatin (show FST Antibodies) is secondary to the action of activin (show Actbeta Antibodies)-C. Study provides evidence to support a role of activin (show Actbeta Antibodies)-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 (show NFATC3 Antibodies) pathway via BMP type I receptor ALK2, contributing to cardiac hypertrophy and fibrosis.
results suggest that ACVR1(R206H) causes FOP (show CHTOP Antibodies) by gaining responsiveness to the normally antagonistic ligand activin A (show INHBA Antibodies), demonstrating that this ligand is necessary and sufficient for driving HO in a genetically accurate model of FOP (show CHTOP Antibodies)
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.
ACVR1 is required for chondrocyte proliferation and differentiation, particularly in craniofacial and axial elements, but exerts coordinated functions with both BMPR1A (show BMPR1A Antibodies) and BMPR1B (show BMPR1B Antibodies) throughout the developing endochondral skeleton
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 (show LIN9 Antibodies)-01 and TGS (show LIN9 Antibodies)-04.
Data suggest BMP9/GDF2 (show GDF2 Antibodies) and BMP10 (show BMP10 Antibodies) synergize with TNFA (show TNF Antibodies) to increase monocyte recruitment to vascular endothelial cells; process appears to be mediated mainly via ALK2/ACVR1 (which exhibits protein kinase (show CDK7 Antibodies) activity). These studies used in vitro flow monocyte adhesion assay. (BMP9 (show GDF2 Antibodies) = growth differentiation factor 2 (show GDF2 Antibodies); BMP10 (show BMP10 Antibodies) = bone morphogenetic protein 10 (show BMP10 Antibodies); TNFA (show TNF Antibodies) = tumor necrosis factor alpha (show TNF Antibodies); 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 (show BMP6 Antibodies), ALK2 and BMPRII (show BMPR2 Antibodies) had deeper growth than tumors with only BMP6 (show BMP6 Antibodies) 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
Activin-A (show INHBA Antibodies) is increased in the airway of asthmatics and peaks during asthma exacerbations.Activin-A signalling pathways are dysregulated in severe asthma.
Common mutations in ALK2/ACVR1, a multi-faceted receptor, have roles in distinct pediatric musculoskeletal and neural orphan disorders.
The higher PE activin A (show INHBA Antibodies) concentrations resulted in abnormal endothelial functions, which may contribute to the systemic maternal vascular endothelial cell dysfunction observed in the disorder.
A report of two patients has been presented with multi-system involvement in a severe variant of fibrodysplasia ossificans progressiva caused by the ACVR1 c.772G>A; R258G mutation.
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