SART-2 CRISPR/Cas9 KO Plasmid (h): sc-407069
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SART-2 CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the SART-2 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SART-2 CRISPR/Cas9 KO Plasmid (h) | sc-407069 | 20 µg | $397.00 |
Overview
DSE encodes dermatan sulfate epimerase, an ER/Golgi-resident enzyme that converts D-glucuronic acid to L-iduronic acid in chondroitin/dermatan sulfate chains, thereby shaping proteoglycan structure and extracellular matrix (ECM) properties. By modulating glycosaminoglycan composition, DSE influences collagen fibrillogenesis, cell–matrix adhesion, and growth factor availability that can impact signaling programs such as TGF-β and other ECM-responsive pathways. Altered dermatan sulfate biosynthesis has been linked to connective tissue phenotypes and dysregulated stromal remodeling, and DSE perturbation is studied in contexts including fibrosis and tumor microenvironment biology. The gene is also referenced in some literature under the protein name SART-2, which may appear in antigen and expression studies depending on annotation conventions.
SART-2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the DSE gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the DSE together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the DSE open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish SART-2 protein expression.
This CRISPR knockout system enables efficient generation of DSE-deficient cell models for investigation of SART-2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting DSE exon(s) critical for SART-2 function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple DSE genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SART-2 CRISPR/Cas9 KO Plasmid (h) and SART-2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the DSE locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SART-2 HDR Plasmid (h) and SART-2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by DSE homology arms to support homology-directed repair at defined DSE target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.