CIRP CRISPR/Cas9 KO Plasmid (m): sc-419664
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CIRP 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 CIRP 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CIRP Antibody (1C9): sc-293325
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CIRP CRISPR/Cas9 KO Plasmid (m) | sc-419664 | 20 µg | $397.00 |
Overview
Cirbp encodes cold-inducible RNA-binding protein (CIRP), a stress-responsive RNA chaperone that modulates mRNA stability, transport, and translation. In mouse cells, CIRP is induced by hypothermia, UV irradiation, hypoxia, and oxidative stress, and it contributes to post-transcriptional gene regulation within stress granules and related ribonucleoprotein complexes. CIRP-linked pathways intersect with cellular stress responses, inflammatory signaling, and circadian and metabolic regulation through selective control of target transcripts. Dysregulated CIRP activity has been associated with altered immune and tissue stress responses, making Cirbp a useful locus for mechanistic studies in inflammation, neurobiology, and cancer-relevant stress adaptation.
CIRP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cirbp gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cirbp 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 Cirbp 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 CIRP protein expression.
This CRISPR knockout system enables efficient generation of Cirbp-deficient cell models for investigation of CIRP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cirbp exon(s) critical for CIRP 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 Cirbp genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CIRP CRISPR/Cas9 KO Plasmid (m) and CIRP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cirbp locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CIRP HDR Plasmid (m) and CIRP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cirbp homology arms to support homology-directed repair at defined Cirbp 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.