Recombinant Mouse Activin RIIA/ACVR2A Protein (His & Fc Tag)(Active) | PKSM040585

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575-PKSM040585
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Description

Recombinant Mouse Activin RIIA/ACVR2A Protein (His & Fc Tag)(Active) | PKSM040585 | Gentaur US, UK & Europe Disrtribition

Synonyms: ActrIIa;Acvr2;TactrII

Active Protein: Active protein

Activity: A DNA sequence encoding the extracellular domain of mouse ACVR2A (NP_031422.3) (Met 1-Pro 134) was fused with the C-terminal polyhistidine-tagged Fc region of human IgG1 at the C-terminus.

Protein Construction: A DNA sequence encoding the extracellular domain of mouse ACVR2A (NP_031422.3) (Met 1-Pro 134) was fused with the C-terminal polyhistidine-tagged Fc region of human IgG1 at the C-terminus.

Fusion Tag: C-His-Fc

Species: Mouse

Expressed Host: HEK293 Cells

Shipping: This product is provided as lyophilized powder which is shipped with ice packs.

Purity: > 97 % as determined by reducing SDS-PAGE.

Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method.

Stability and Storage: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.

Molecular Mass: 41.4 kDa

Formulation: Lyophilized from sterile PBS, pH 7.4

Reconstitution: Please refer to the printed manual for detailed information.

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.

Research Area: N/A

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