GSTM5 CRISPR/Cas9 KO Plasmid (h): sc-406828
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GSTM5 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 GSTM5 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 | |
GSTM5 CRISPR/Cas9 KO Plasmid (h) | sc-406828 | 20 µg | $397.00 |
Overview
GSTM5 encodes glutathione S-transferase mu 5 (GSTM5), a phase II detoxification enzyme that catalyzes the conjugation of reduced glutathione to electrophilic compounds, supporting cellular defense against xenobiotics and reactive oxygen species. As part of the glutathione-dependent redox network, GSTM5 contributes to maintaining proteostasis and limiting oxidative damage to lipids, proteins, and DNA. Variation or dysregulation of GSTM family activity has been associated with altered susceptibility to oxidative stress and inflammatory signaling, processes frequently implicated in carcinogenesis and tissue injury. In human cells, GSTM5 is often studied in the context of chemical metabolism, environmental exposure responses, and mechanisms that shape cellular redox homeostasis.
GSTM5 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the GSTM5 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the GSTM5 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 GSTM5 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 GSTM5 protein expression.
This CRISPR knockout system enables efficient generation of GSTM5-deficient cell models for investigation of GSTM5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting GSTM5 exon(s) critical for GSTM5 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 GSTM5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by GSTM5 CRISPR/Cas9 KO Plasmid (h) and GSTM5 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the GSTM5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by GSTM5 HDR Plasmid (h) and GSTM5 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by GSTM5 homology arms to support homology-directed repair at defined GSTM5 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.