ZRSR2 CRISPR/Cas9 KO Plasmid (m): sc-423571
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZRSR2 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 ZRSR2 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 | |
ZRSR2 CRISPR/Cas9 KO Plasmid (m) | sc-423571 | 20 µg | $397.00 |
Overview
Zrsr2 encodes ZRSR2, a zinc finger RNA-binding protein that functions as a core component of the spliceosome with a prominent role in recognition and removal of U12-type introns. Through regulation of pre-mRNA splicing fidelity, ZRSR2 influences transcript isoform choice and the expression of genes involved in cell-cycle control, differentiation, and stress responses. Disruption of ZRSR2-dependent minor spliceosome activity can lead to aberrant intron retention and widespread RNA processing defects, linking this pathway to altered hematopoietic and immune cell programs in disease-relevant contexts. As a conserved splicing factor, mouse ZRSR2 is useful for mechanistic studies of spliceosomal assembly, minor intron biology, and downstream proteome remodeling.
ZRSR2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Zrsr2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Zrsr2 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 Zrsr2 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 ZRSR2 protein expression.
This CRISPR knockout system enables efficient generation of Zrsr2-deficient cell models for investigation of ZRSR2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Zrsr2 exon(s) critical for ZRSR2 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 Zrsr2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ZRSR2 CRISPR/Cas9 KO Plasmid (m) and ZRSR2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Zrsr2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ZRSR2 HDR Plasmid (m) and ZRSR2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Zrsr2 homology arms to support homology-directed repair at defined Zrsr2 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.