Human ACVR2 / ACTRII / ACVR2A Protein (Fc Tag)
ACTRII,ACVR2
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Catalog Number | P10257-H02H |
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Organism Species | Human |
Host | Human Cells |
Synonyms | ACTRII,ACVR2 |
Molecular Weight | The recombinant human ACVR2A/Fc chimera is a disulfide-linked homodimer protein generated after removal of the signal peptide. The monomer comprises 352 amino acids and predicts a molecular mass of 40.0 kDa. As a result of glycosylation, the monomer migrates as an approximately 60-65 kDa protein in SDS-PAGE under reducing conditions. |
predicted N | Ala 20 |
SDS-PAGE | |
Purity | > 97 % as determined by SDS-PAGE |
Protein Construction | A DNA sequence encoding the N-terminal segment (Met 1-Pro 134) from the extracellular domain of human ACVR2A (NP_001607.1) was fused with the Fc region of human IgG1 at the C-terminus. |
Bio-activity | Measured by its ability to neutralize Activin-mediated inhibition on MPC11 cell proliferation. The ED50 for this effect is typically 10-40 ng/mL in the presence of 10 ng/mL recombinant Activin A. |
Research Area | Cancer |Invasion microenvironment |Angiogenesis |Growth Factor & Receptor |Transforming Growth Factor Beta (TGF-beta) Superfamily |TGF-beta Superfamily Receptors | |
Formulation | Lyophilized from sterile PBS, pH 7.4 1. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA. |
Background | ACVR2A and ACVR2B are two activin type II receptors. ACVR2A has been shown to interact with INHBA, SYNJ2BP and ACVR1B. The bovine ACVR2A gene encodes a protein of 513 amino acids which is highly homologous (approximately 98% identity) to the rat, mouse, and human ACVR2A proteins. Inactivation of ACVR2A is a common event in prostate cancer cells suggesting it may play an important role in the development of prostate cancer. The ACVR2A gene is a putative tumor suppressor gene that is frequently mutated in microsatellite-unstable colon cancers (MSI-H colon cancers). Frameshift mutation of ACVR2A may contribute to MSI-H colon tumorigenesis via disruption of alternate TGF-beta effector pathways. |
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