DHRS3 CRISPR/Cas9 KO Plasmid (h): sc-411259
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DHRS3 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 DHRS3 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 | |
DHRS3 CRISPR/Cas9 KO Plasmid (h) | sc-411259 | 20 µg | $397.00 |
Overview
DHRS3 (dehydrogenase/reductase 3) encodes an NADPH-dependent short-chain dehydrogenase/reductase that catalyzes the reduction of retinaldehyde to retinol, helping regulate intracellular retinoid homeostasis. By limiting the availability of retinal for oxidation to retinoic acid, DHRS3 modulates retinoic acid signaling programs that influence differentiation, embryonic development, epithelial biology, and metabolic adaptation. DHRS3 expression is responsive to retinoids and integrates with retinol storage and oxidative stress-related processes through control of reactive aldehyde flux. Dysregulated retinoid metabolism and altered DHRS3 activity have been associated with developmental abnormalities and cancer-related changes in differentiation states, making it relevant for mechanistic studies of retinoid-driven phenotypes.
DHRS3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the DHRS3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the DHRS3 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 DHRS3 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 DHRS3 protein expression.
This CRISPR knockout system enables efficient generation of DHRS3-deficient cell models for investigation of DHRS3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting DHRS3 exon(s) critical for DHRS3 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 DHRS3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by DHRS3 CRISPR/Cas9 KO Plasmid (h) and DHRS3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the DHRS3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by DHRS3 HDR Plasmid (h) and DHRS3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by DHRS3 homology arms to support homology-directed repair at defined DHRS3 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.