Cyclophilin 40 CRISPR/Cas9 KO Plasmid (m): sc-426720
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cyclophilin 40 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 Cyclophilin 40 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: Cyclophilin 40 Antibody (C-11): sc-137216
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cyclophilin 40 CRISPR/Cas9 KO Plasmid (m) | sc-426720 | 20 µg | $397.00 |
Overview
Ppid encodes cyclophilin 40 (Cyp40), a peptidyl-prolyl cis–trans isomerase that functions as a TPR-domain co-chaperone within HSP90/HSP70 complexes. By facilitating conformational maturation and assembly of client proteins, Cyp40 influences proteostasis, steroid receptor signaling, and stress-responsive pathways linked to protein folding and quality control. Ppid has also been associated with regulation of mitochondrial protein handling and apoptotic susceptibility through chaperone-dependent mechanisms. Dysregulation of chaperone–immunophilin networks is frequently studied in contexts of neurodegeneration, inflammation, and cancer-associated proteome stress, making Ppid a useful node for mechanistic interrogation in mouse systems.
Cyclophilin 40 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ppid gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ppid 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 Ppid 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 Cyclophilin 40 protein expression.
This CRISPR knockout system enables efficient generation of Ppid-deficient cell models for investigation of Cyclophilin 40 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ppid exon(s) critical for Cyclophilin 40 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 Ppid genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Cyclophilin 40 CRISPR/Cas9 KO Plasmid (m) and Cyclophilin 40 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ppid locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Cyclophilin 40 HDR Plasmid (m) and Cyclophilin 40 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ppid homology arms to support homology-directed repair at defined Ppid 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.