CLC-7 CRISPR/Cas9 KO Plasmid (h): sc-404550
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLC-7 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 CLC-7 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 | |
CLC-7 CRISPR/Cas9 KO Plasmid (h) | sc-404550 | 20 µg | $397.00 |
Overview
CLCN7 encodes CLC-7, a voltage-gated Cl⁻/H⁺ antiporter predominantly localized to late endosomes and lysosomes where it supports organellar acidification and ionic homeostasis. By coupling chloride flux to the V-ATPase proton gradient, CLC-7 regulates lysosomal degradative capacity, endolysosomal trafficking, and autophagy-lysosome pathway function. CLCN7 activity is particularly important in osteoclasts for resorption lacuna acidification and bone matrix turnover, and perturbation of CLC-7–dependent lysosomal physiology is linked to skeletal and neurodegenerative phenotypes. These properties make CLCN7 a useful target for studying lysosome biology, ion transport in intracellular membranes, and cell-type–specific contributions to tissue homeostasis.
CLC-7 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CLCN7 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CLCN7 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 CLCN7 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 CLC-7 protein expression.
This CRISPR knockout system enables efficient generation of CLCN7-deficient cell models for investigation of CLC-7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CLCN7 exon(s) critical for CLC-7 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 CLCN7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CLC-7 CRISPR/Cas9 KO Plasmid (h) and CLC-7 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CLCN7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CLC-7 HDR Plasmid (h) and CLC-7 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CLCN7 homology arms to support homology-directed repair at defined CLCN7 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.