Recombinant Mouse VSTM2A His-tag Protein, CF Summary
Ser25-Ala252, with a C-terminal 6-His tag
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS.|
|Reconstitution||Reconstitute at 100 μg/mL in PBS.|
|Shipping||The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||
2 μg/lane of Recombinant Mouse VSTM2A was resolved with SDS-PAGE underreducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Bluestaining, showing bands at 35-44 kDa.
V-set and transmembrane domain-containing protein 2A (VSTM2A) is a secreted glycoprotein that is expressed by committed preadipocytes. N-linked glycosylation is crucial for its secretion, but not for preadipocyte cell differentiation activity. It is expressed during adipocyte development and its over-expression promotes adipogenesis (1). VSTM2A is highly expressed in the brain and Vstm2a was identified as an enigmatic gene that is highly produced in mouse brain (1, 2). A positive association has been observed between Vstm2a and Pparg2. PPAR gamma 2 indirectly promotes Vstm2a expression in preadipocytes by amplifying adipogenic commitment, while VSTM2A promotes Pparg2 expression by activating BMP signaling (1, 3). VSTM2A is synthesized as a precursor protein that contains a 24 amino acid (aa) signal sequence followed by the VSTM2A domain. The mouse VSTM2A shares 78% and 99% aa sequence identity with human and rat VSTM2A, respectively. Adipogenic commitment was uninhibited by over-expression of VSTM2A lacking a signal peptide for secretion, suggesting that secreted VSTM2A is not involved in adipogenic commitment in vitro. While the exact role secreted VSTM2A plays is unknown, it is suggested it may modulate angiogenesis or neurogenesis due to its expression in the brain and near blood vessels, and the need for adipose tissue to develop alongside blood vessels and neural tissue (1, 4). Our data shows that mouse VSTM2A inhibits anti-CD3 induced IFN-gamma secretion in Human T cells.
- Secco, B. et al. (2017) Cell Rep. 18:93.
- Pandey, A.K. et al. (2014) PloS One. 9:e88889.
- Berry, D.C. et al. (2013) Development. 140:3939.
- Nishimura, S. et al. (2007) Diabetes. 56:1517.
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