Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CA IV CRISPR/Cas9 KO Plasmid (m): sc-419454
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CA IV 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 CA IV 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: CA IV Antibody (H-5): sc-74446
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CA IV CRISPR/Cas9 KO Plasmid (m) | sc-419454 | 20 µg | $397.00 |
Overview
Mouse Car4 encodes carbonic anhydrase IV (CA IV), a GPI-anchored extracellular enzyme that catalyzes the reversible hydration of CO₂ to bicarbonate and protons, supporting local pH regulation and bicarbonate transport. By functionally coupling to ion transport processes, CA IV contributes to CO₂/HCO₃⁻ homeostasis that influences epithelial and endothelial physiology, gas exchange, and microenvironmental acid–base balance. Car4 activity is commonly studied in the context of pulmonary and renal bicarbonate handling as well as tissue responses to altered pH and CO₂ levels. Dysregulated carbonic anhydrase-dependent buffering can impact processes linked to inflammation, hypoxia-associated remodeling, and metabolic stress pathways.
CA IV CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Car4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Car4 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 Car4 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 CA IV protein expression.
This CRISPR knockout system enables efficient generation of Car4-deficient cell models for investigation of CA IV signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Car4 exon(s) critical for CA IV 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 Car4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CA IV CRISPR/Cas9 KO Plasmid (m) and CA IV CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Car4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CA IV HDR Plasmid (m) and CA IV HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Car4 homology arms to support homology-directed repair at defined Car4 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.