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ACVR1 Antibody (Center)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q04771 |
| Other Accession | P80201, P37172, Q28041, NP_001104537.1, NP_001096.1 |
| Reactivity | Human |
| Predicted | Bovine, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 57153 Da |
| Antigen Region | 132-161 aa |
| Gene ID | 90 |
|---|---|
| Other Names | Activin receptor type-1, Activin receptor type I, ACTR-I, Activin receptor-like kinase 2, ALK-2, Serine/threonine-protein kinase receptor R1, SKR1, TGF-B superfamily receptor type I, TSR-I, ACVR1, ACVRLK2 |
| Target/Specificity | This ACVR1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 132-161 amino acids from the Central region of human ACVR1. |
| Dilution | WB~~1:2000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | ACVR1 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | ACVR1 |
|---|---|
| Synonyms | ACVRLK2 |
| Function | Bone morphogenetic protein (BMP) type I receptor that is involved in a wide variety of biological processes, including bone, heart, cartilage, nervous, and reproductive system development and regulation (PubMed:20628059, PubMed:22977237). As a type I receptor, forms heterotetrameric receptor complexes with the type II receptors AMHR2, ACVR2A or ACVR2B (PubMed:17911401). Upon binding of ligands such as BMP7 or GDF2/BMP9 to the heteromeric complexes, type II receptors transphosphorylate ACVR1 intracellular domain (PubMed:25354296). In turn, ACVR1 kinase domain is activated and subsequently phosphorylates SMAD1/5/8 proteins that transduce the signal (PubMed:9748228). In addition to its role in mediating BMP pathway-specific signaling, suppresses TGFbeta/activin pathway signaling by interfering with the binding of activin to its type II receptor (PubMed:17911401). Besides canonical SMAD signaling, can activate non-canonical pathways such as p38 mitogen-activated protein kinases/MAPKs (By similarity). May promote the expression of HAMP, potentially via its interaction with BMP6 (By similarity). |
| Cellular Location | Membrane; Single-pass type I membrane protein. |
| Tissue Location | Expressed in normal parenchymal cells, endothelial cells, fibroblasts and tumor-derived epithelial cells |
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Provided below are standard protocols that you may find useful for product applications.
Background
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.
References
Canzian, F., et al. Hum. Mol. Genet. 19(19):3873-3884(2010)
Shimada, M., et al. Hum. Genet. 128(4):433-441(2010)
Song, G.A., et al. J. Biol. Chem. 285(29):22542-22553(2010)
Herrera, B., et al. Cancer Res. 69(24):9254-9262(2009)
Jung, B., et al. PLoS ONE 4 (12), E8308 (2009) :
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