Recombinant Human DGCR2 His-tag Protein, CF Summary
Glu22-Ala349, with an C-terminal 6-His tag
CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS.|
|Reconstitution||Reconstitute at 500 μg/mL in PBS.|
|Shipping||The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
2 μg/lane of Recombinant Human DGCR2 His-tag (Catalog # 10161-DG) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing bands at 40-60 kDa.
DiGeorge Syndrome Critical Region 2 (DGCR2), also known as IDD, DGS-C, LAN, and SEZ-12, is an adhesion receptor protein located on the long arm of chromosome 22 (1). The DGCR2 gene encodes an integral membrane protein, consisting of an extracellular domain, a single transmembrane region and a cytoplasmic tail (1). The mature extracellular domain (ECD) of DGCR2 contains both a C-type lectin domain and a cysteine-rich region similar to that of the low density lipoprotein receptor (LDLR) (1, 3). The mature ECD of human DGCR2 shares 93% and 92% amino acid sequence identity with mouse and rat, respectively. DGCR2 is expressed during neurodevelopment in human brain tissues (3). Deletion of the 22q11.2 region results in an extremely variable disorder called 22q11.2 deletion syndrome, with a phenotype ranging from very mild symptoms to severe intellectual disability, facial dysmorphism, heart defects, and urogenital abnormalities (4). Recent studies suggest that DGCR2 regulates critical steps of early cortico-genesis possibly through a Reelin-dependent mechanism. Deletion of DGCR2 has a pathogenic impact on cortical formation by reducing protein expression level, and it plays a critical role in vulnerability to schizophrenia (5). Furthermore, expression of DGCR2 together with USP18 gene may serve as a progonostic marker for muscle invasive bladder cancer survival in patients (5).
- Augusseau, S. et al. (1986) Hum. Genet. 74:206.
- Mugikura, S. et al. (2016) Biochem Biophys Rep. 5:120.
- Kajiwara, K. et al. (1996) Biochem. Biophyis. Res. Commun. 222:144.
- Vaisvilas, M. et al. (2018) Balkan J Med Genet. 21:87.
- Molinard-Chenu A. and Dayer A. (2017) Biol. Psych. 83:692.
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