Activin Receptor Type I (ACRV1) ELISA Kits

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 (182) and Activin Receptor Type I Proteins (35) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
ACRV1 90 Q04771
ACRV1 79558 P80201
ACRV1 11477 P37172
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Top Activin Receptor Type I ELISA Kits at

Showing 10 out of 16 products:

Catalog No. Reactivity Sensitivity Range Images Quantity Supplier Delivery Price Details
Human 0.054 ng/mL 0.15 ng/mL - 10 ng/mL 96 Tests Log in to see 13 to 16 Days
Mouse 0.1 ng/mL 0.5-10 ng/mL   96 Tests Log in to see 15 to 18 Days
Dog 0.1 ng/mL 0.5-10 ng/mL   96 Tests Log in to see 15 to 18 Days
Rat 0.1 ng/mL 250-5000 pg/mL   96 Tests Log in to see 15 to 18 Days
Guinea Pig 0.1 ng/mL 0.5-10 ng/mL   96 Tests Log in to see 15 to 18 Days
Monkey 0.1 ng/mL 0.5-10 ng/mL   96 Tests Log in to see 15 to 18 Days
  96 Tests Log in to see 15 to 18 Days
  96 Tests Log in to see 15 to 18 Days
  96 Tests Log in to see 15 to 18 Days
  96 Tests Log in to see 15 to 18 Days

More ELISA Kits for Activin Receptor Type I Interaction Partners

Human Activin Receptor Type I (ACRV1) interaction partners

  1. this study characterized the ALK2 mutants R258G, G328V and F246Y, which were identified in patients with severe fibrodysplasia ossificans progressiva, diffuse intrinsic pontine glioma and unusual hereditary skeletal dysplasia, respectively.

  2. Identification of small molecule inhibitors of ALK2: a virtual screening, density functional theory, and molecular dynamics simulations study.

  3. Results showed that ACVR1 was a direct target of miR-384 and was involved in the inhibitory effects of miR-384 on breast cancer progression. Furthermore, the study indicated that ACVR1 activated the Wnt/beta-catenin signaling pathway in breast cancer.

  4. 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. [review]

  5. The role of an ALK2 mutation (R258S) in IRIDA development in a patient also bearing compound heterozygous mutations in TMPRSS6 was demonstrated by reconstructing in vitro the proband's genotype, expressing mutants TMPRSS6 and ACVR1 in the presence of hemojuvelin and assessing hepcidin activation. ALK2(R258S) maintained high hepcidin expression in the presence of MT2(I212T).

  6. activation of AMPK upregulated Smad6 and Smurf1 and thereby enhanced their interactions, resulting in its proteosome-dependent degradation of ALK2.

  7. the Fibrodysplasia Ossificans Progressiva mutation ACVR1(R206H) is more sensitive to a number of natural ligands.

  8. both bone morphogenetic protein 2 (BMP2) and BMP6 are proangiogenic in vitro and ex vivo and that the BMP type I receptors, activin receptor-like kinase 3 (ALK3) and ALK2, play crucial and distinct roles in this process.

  9. 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.

  10. The ACVR1 R206H mutation may not directly increase the formation of mature chondrogenic or osteogenic cells.

  11. 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.

  12. Data suggest BMP9/GDF2 and BMP10 synergize with TNFA to increase monocyte recruitment to vascular endothelial cells; process appears to be mediated mainly via ALK2/ACVR1 (which exhibits protein kinase activity). These studies used in vitro flow monocyte adhesion assay. (BMP9 = growth differentiation factor 2; BMP10 = bone morphogenetic protein 10; TNFA = tumor necrosis factor alpha; ALK2/ACVR1 = activin A receptor type 1)

  13. 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.

  14. Low ALK2 expression is associated with invasiveness of breast cancer.

  15. Further investigation on clinical ESCC samples and non-tumorous adjacent tissue found that tumors with triple-positive BMP6, ALK2 and BMPRII had deeper growth than tumors with only BMP6 expression

  16. 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

  17. Activin-A is increased in the airway of asthmatics and peaks during asthma exacerbations.Activin-A signalling pathways are dysregulated in severe asthma.

  18. Common mutations in ALK2/ACVR1, a multi-faceted receptor, have roles in distinct pediatric musculoskeletal and neural orphan disorders.

  19. The higher PE activin A concentrations resulted in abnormal endothelial functions, which may contribute to the systemic maternal vascular endothelial cell dysfunction observed in the disorder.

  20. 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.

Mouse (Murine) Activin Receptor Type I (ACRV1) interaction partners

  1. This study demonstrates for the first time the physiological roles of ACVR1 during dentinogenesis.

  2. Systemic activation of Activin A signaling causes chronic kidney disease-mineral bone disorder. (Review)

  3. findings demonstrate that hair follicle specific ALK2 is intricately involved in maintenance of the stem cell niche and wound healing

  4. targeted expression to fibro/adipogenic progenitors recapitulates the full spectrum of heterotopic ossification observed in fibrodysplasia ossificans progressiva patients

  5. NODAL/Activin signaling induces dramatic chromatin landscape changes, and a dynamic transcriptional network regulated by SMAD2, acting via multiple mechanisms.

  6. Acute tacrolimus treatment transiently increases hepcidin in wild-type mice. FKBP12 preferentially targets the BMP receptor ALK2. ALK2 mutants defective in binding FKBP12 increase hepcidin expression in a ligand-independent manner, through BMP-SMAD signaling.

  7. The authors demonstrated that ubiquitin-specific protease (USP) 4 strongly induces activin/BMP signaling by removing the inhibitory monoubiquitination from SMAD4.

  8. Enhanced SMAD-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.

  9. BMP signaling mediated by coordination of ALK2/ACVR1, ALK3/BMPR1A, and BMPR2 is an essential proangiogenic cue for retinal vessels.

  10. This study showed that Gja1 may act downstream of cAMP-PKA signal to mediate the effects of Acvr1 on the differentiation of uterine stromal cells through targeting Hand2.

  11. Results showed activin-C and follistatin are differentially expressed during prostate development and suggested that the antagonistic property of follistatin is secondary to the action of activin-C. Study provides evidence to support a role of activin-C in prostate development and provides new insights in the spatiotemporal localization of activins and their antagonists during mouse prostate development.

  12. BMPR1B plays distinct roles from BMPR1A and ACVR1 in maintaining bone mass and transducing BMP signaling

  13. Suggest that BMP signaling upregulates the calcineurin/nuclear factor of activated T cell pathway via BMP type I receptor ALK2, contributing to cardiac hypertrophy and fibrosis.

  14. results suggest that ACVR1(R206H) causes FOP by gaining responsiveness to the normally antagonistic ligand activin A, demonstrating that this ligand is necessary and sufficient for driving HO in a genetically accurate model of FOP

  15. 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.

  16. ACVR1 is required for chondrocyte proliferation and differentiation, particularly in craniofacial and axial elements, but exerts coordinated functions with both BMPR1A and BMPR1B throughout the developing endochondral skeleton

  17. expression of constitutively active ALK2 receptor results in significantly increased ASC osteogenic differentiation.

  18. SP-10 is a useful marker for staging the cycle of the seminiferous epithelium. The anti-SP-10 antibody works well in different fixatives, on paraffin-embedded as well as cryosections

  19. Data indicate that activin A receptor type 1 (Alk2) is a direct regulator of cartilage formation and mediates chondrogenic commitment of progenitor cells.

  20. Tmem176b mRNA levels were upregulated by stable transfection of ALK2 (R206H) in mouse myoblastic C2C12 cells.

Horse (Equine) Activin Receptor Type I (ACRV1) interaction partners

  1. 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.

Activin Receptor Type I (ACRV1) Antigen Profile

Antigen Summary

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.

Gene names and symbols associated with ACRV1

  • activin A receptor type 1 (ACVR1) antibody
  • activin A receptor type 1 (Acvr1) antibody
  • activin A receptor, type 1 (Acvr1) antibody
  • activin A receptor type 1 S homeolog (acvr1.S) antibody
  • ActR-I antibody
  • ActR-IA antibody
  • actri antibody
  • ActRIA antibody
  • Acvr antibody
  • acvr1 antibody
  • acvr1-a antibody
  • acvr1-b antibody
  • acvr1a antibody
  • acvrlk2 antibody
  • alk-2 antibody
  • alk2 antibody
  • alk8 antibody
  • D330013D15Rik antibody
  • fop antibody
  • sax antibody
  • skr1 antibody
  • Tsk7L antibody
  • tsri antibody
  • xALK-2 antibody

Protein level used designations for ACRV1

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 , ACTR-I , SKR1 , TSR-I , activin A receptor, type 1 , activin type I receptor , type I TGF B receptor , activin A receptor, type I , activin receptor type IA , TSK-7L , activin A receptor type 1 S homeolog , activin A receptor type I S homeolog , activin receptor like kinase-2

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