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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 (16) and many more products for this protein.
Showing 10 out of 179 products:
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 3 Pubmed References
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 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
Human Polyclonal ACRV1 Primary Antibody for WB - ABIN391156
Kan, Liu, McGuire, Berger, Awatramani, Dymecki, Kessler: Dysregulation of local stem/progenitor cells as a common cellular mechanism for heterotopic ossification. in Stem cells (Dayton, Ohio) 2009
Results showed that ACVR1 was a direct target of miR (show MLXIP Antibodies)-384 and was involved in the inhibitory effects of miR (show MLXIP Antibodies)-384 on breast cancer progression. Furthermore, the study indicated that ACVR1 activated the Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling pathway in breast cancer.
Study emphasizes about the role of ACVR1 which encoding a receptor for BMP proteins in fibrodysplasia ossificans progressiva (FOP). Most FOP patients carry the recurrent R206H substitution in the GS domain, whereas a few other mutations are responsible for limited cases. Mutations cause a dysregulation of the downstream BMP-dependent pathway making mutated ACVR1 responsive to a non-canonical ligand, Activin A (show INHBA Antibodies). [review]
The role of an ALK2 mutation (R258S) in IRIDA (show TMPRSS6 Antibodies) development in a patient also bearing compound heterozygous mutations in TMPRSS6 (show TMPRSS6 Antibodies) was demonstrated by reconstructing in vitro the proband's genotype, expressing mutants TMPRSS6 (show TMPRSS6 Antibodies) and ACVR1 in the presence of hemojuvelin (show HFE2 Antibodies) and assessing hepcidin (show HAMP Antibodies) activation. ALK2(R258S) maintained high hepcidin (show HAMP Antibodies) expression in the presence of MT2 (show MT2 Antibodies)(I212T).
activation of AMPK (show PRKAA1 Antibodies) upregulated Smad6 (show SMAD6 Antibodies) and Smurf1 (show SMURF1 Antibodies) and thereby enhanced their interactions, resulting in its proteosome-dependent degradation of ALK2.
the Fibrodysplasia Ossificans Progressiva mutation ACVR1(R206H) is more sensitive to a number of natural ligands.
both bone morphogenetic protein 2 (BMP2 (show BMP2 Antibodies)) and BMP6 (show BMP6 Antibodies) are proangiogenic in vitro and ex vivo and that the BMP type I receptors, activin receptor-like kinase 3 (ALK3 (show BMPR1A Antibodies)) 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 (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)
findings demonstrate that hair follicle specific ALK2 is intricately involved in maintenance of the stem cell niche and wound healing
NODAL/Activin (show Actbeta Antibodies) signaling induces dramatic chromatin landscape changes, and a dynamic transcriptional network regulated by SMAD2 (show SMAD2 Antibodies), acting via multiple mechanisms.
Acute tacrolimus treatment transiently increases hepcidin (show HAMP Antibodies) in wild-type mice. FKBP12 (show FKBP1A Antibodies) preferentially targets the BMP receptor (show BMPR1A Antibodies) ALK2. ALK2 mutants defective in binding FKBP12 (show FKBP1A Antibodies) increase hepcidin (show HAMP Antibodies) expression in a ligand-independent manner, through BMP-SMAD (show SMAD1 Antibodies) signaling.
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.
Data suggest that ACVR1 mRNA and protein are present in granulosa cells of ovarian follicles at mid-estrous and pre-ovulatory stages; ACVR1 mRNA and protein are also present in exosomes isolated from mid-estrous and preovulatory follicles.
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 A receptor, type II-like kinase 2
, activin receptor type I
, activin receptor type-1
, activin receptor-like kinase 2
, hydroxyalkyl-protein kinase
, serine/threonine-protein kinase receptor R1
, activin A receptor, type 1
, activin type I receptor
, type I TGF B receptor
, activin A receptor, type I
, activin receptor type IA
, activin A receptor type 1 S homeolog
, activin A receptor type I S homeolog
, activin receptor like kinase-2