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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 Antibodies (176) and Activin Receptor Type I Proteins (35) and many more products for this protein.
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The role of an ALK2 mutation (R258S) in IRIDA (show TMPRSS6 ELISA Kits) development in a patient also bearing compound heterozygous mutations in TMPRSS6 (show TMPRSS6 ELISA Kits) was demonstrated by reconstructing in vitro the proband's genotype, expressing mutants TMPRSS6 (show TMPRSS6 ELISA Kits) and ACVR1 in the presence of hemojuvelin (show HFE2 ELISA Kits) and assessing hepcidin (show HAMP ELISA Kits) activation. ALK2(R258S) maintained high hepcidin (show HAMP ELISA Kits) expression in the presence of MT2 (show MT2 ELISA Kits)(I212T).
activation of AMPK (show PRKAA1 ELISA Kits) upregulated Smad6 (show SMAD6 ELISA Kits) and Smurf1 (show SMURF1 ELISA Kits) 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 ELISA Kits)) and BMP6 (show BMP6 ELISA Kits) are proangiogenic in vitro and ex vivo and that the BMP type I receptors, activin receptor-like kinase 3 (ALK3 (show BMPR1A ELISA Kits)) 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-01 and TGS-04.
Data suggest BMP9/GDF2 (show GDF2 ELISA Kits) and BMP10 (show BMP10 ELISA Kits) synergize with TNFA (show TNF ELISA Kits) to increase monocyte recruitment to vascular endothelial cells; process appears to be mediated mainly via ALK2/ACVR1 (which exhibits protein kinase (show CDK7 ELISA Kits) activity). These studies used in vitro flow monocyte adhesion assay. (BMP9 (show GDF2 ELISA Kits) = growth differentiation factor 2 (show GDF2 ELISA Kits); BMP10 (show BMP10 ELISA Kits) = bone morphogenetic protein 10 (show BMP10 ELISA Kits); TNFA (show TNF ELISA Kits) = tumor necrosis factor alpha (show TNF ELISA Kits); 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.
findings demonstrate that hair follicle specific ALK2 is intricately involved in maintenance of the stem cell niche and wound healing
NODAL/Activin (show Actbeta ELISA Kits) signaling induces dramatic chromatin landscape changes, and a dynamic transcriptional network regulated by SMAD2 (show SMAD2 ELISA Kits), acting via multiple mechanisms.
Acute tacrolimus treatment transiently increases hepcidin (show HAMP ELISA Kits) in wild-type mice. FKBP12 (show FKBP1A ELISA Kits) preferentially targets the BMP receptor (show BMPR1A ELISA Kits) ALK2. ALK2 mutants defective in binding FKBP12 (show FKBP1A ELISA Kits) increase hepcidin (show HAMP ELISA Kits) expression in a ligand-independent manner, through BMP-SMAD (show SMAD1 ELISA Kits) signaling.
The authors demonstrated that ubiquitin-specific protease (USP) 4 strongly induces activin (show Actbeta ELISA Kits)/BMP signaling by removing the inhibitory monoubiquitination from SMAD4 (show SMAD4 ELISA Kits).
Enhanced SMAD (show SMAD1 ELISA Kits)-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 ELISA Kits), and BMPR2 (show BMPR2 ELISA Kits) is an essential proangiogenic cue for retinal vessels.
This study showed that Gja1 (show GJA1 ELISA Kits) 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 ELISA Kits).
Results showed activin (show Actbeta ELISA Kits)-C and follistatin (show FST ELISA Kits) are differentially expressed during prostate development and suggested that the antagonistic property of follistatin (show FST ELISA Kits) is secondary to the action of activin (show Actbeta ELISA Kits)-C. Study provides evidence to support a role of activin (show Actbeta ELISA Kits)-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 ELISA Kits) 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