CHP CRISPR/Cas9 KO Plasmid (h): sc-406233
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CHP 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 CHP 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 | |
CHP CRISPR/Cas9 KO Plasmid (h) | sc-406233 | 20 µg | $397.00 |
Overview
CHP1 encodes calcineurin B homologous protein (CHP), a myristoylated EF-hand Ca2+-binding regulator that associates with multiple membrane transporters and signaling proteins. CHP is best known for modulating Na+/H+ exchanger activity, thereby linking intracellular Ca2+ dynamics to pH homeostasis, ion transport, and control of cell volume and cytoskeletal organization. Through these functions it can influence pathways governing epithelial polarity, proliferation, and stress responses. Dysregulated Ca2+ signaling and exchanger regulation involving CHP1 have been investigated in contexts such as tumor cell behavior and other disorders where altered ion balance and pH regulation contribute to pathophysiology.
CHP CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CHP1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CHP1 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 CHP1 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 CHP protein expression.
This CRISPR knockout system enables efficient generation of CHP1-deficient cell models for investigation of CHP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CHP1 exon(s) critical for CHP 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 CHP1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CHP CRISPR/Cas9 KO Plasmid (h) and CHP CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CHP1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CHP HDR Plasmid (h) and CHP HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CHP1 homology arms to support homology-directed repair at defined CHP1 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.