Recombinant Human DSPG3 Protein, CF Summary
Optimal dilutions should be determined by each laboratory for each application.
Met1-Val322 with a C-terminal 10-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 200 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.
Human DSPG3 (dermatan sulfate proteoglycan 3), also called epiphycan (gene name EPYC) or PG-Lb, is a 95-100 kDa class III subfamily member of the SLRP (small leucine-rich proteoglycans) family of molecules (1-4). It is synthesized as a 322 amino acid (aa) precursor that contains a 19 aa signal sequence and a 303 aa mature region. The mature molecule contains three N-terminal O-glycosylation sites (including one found to bind dermatin sulfate) and a glutamic acid-rich motif followed by six leucine-rich repeats (LRR) that contain two potential N-glycosylation sites (2, 3). The LRR are flanked by two intrachain disulfide bonds (5). Class III SLRPs, including DSPG3, Osteoglycin and Opticin, contain 6-7 LRR, while other classes contain 8 ‑ 10 LRR (1, 4). Collagen binding maps to the LRR (1). Mature human DSPG3 shares 84%, 85%, 95% and 96% aa sequence identity with mouse, rat, bovine and canine DSPG3, respectively. DSPG3 is found predominantly in epiphyseal cartilage, although DSPG3 mRNA is also detected in mouse testis and human ligament and placenta (2-4). In mouse, expression begins in mid-gestation as an intermediate marker for chondrogenesis, peaks at birth and declines thereafter (6, 7). Deletion of DSPG3 in mouse results in a mild postnatal phenotype that worsens synergistically when the co‑expressed SLRP biglycan is also deleted (7). The double-mutant phenotype includes premature osteoarthritis, indicating a role for DSPG3, in cooperation with other SLRPs, in stability of the collagen matrix and maintenance of joint integrity (7).
- Kalamajski, S. and A. Oldberg (2010) Matrix Biol. 29:248.
- Kurita, K. et al. (1996) Biochem. J. 318:909.
- Deere, M. et al. (1996) Genomics 38:399.
- Deere, M. et al. (1999) Genome Res. 9:449.
- Swiss-Prot Accession # Q96645 and P70186.
- Johnson, J. et al. (1999) Dev. Dyn. 216:499.
- Nuka, S. et al. (2010) Osteoarthritis Cartilage 18:88.
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