TRPC4 CRISPR/Cas9 KO Plasmid (m): sc-423515
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRPC4 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 TRPC4 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 | |
TRPC4 CRISPR/Cas9 KO Plasmid (m) | sc-423515 | 20 µg | $397.00 |
Overview
Trpc4 encodes TRPC4, a nonselective cation channel of the canonical TRP family that mediates receptor-operated and store-operated Ca²⁺ entry downstream of GPCR and PLC signaling. TRPC4-dependent Ca²⁺ influx contributes to membrane depolarization and calcium-dependent transcriptional programs, influencing processes such as endothelial barrier regulation, smooth muscle contractility, and neuronal excitability. In mouse systems, TRPC4 activity is commonly studied in pathways controlling vascular tone and permeability, gastrointestinal and urinary tract motility, and synaptic signaling. Dysregulated TRPC4-linked calcium homeostasis has been associated with phenotypes relevant to cardiovascular, inflammatory, and neurobehavioral research, supporting its use as a mechanistic node in signaling and physiology studies.
TRPC4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trpc4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trpc4 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 Trpc4 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 TRPC4 protein expression.
This CRISPR knockout system enables efficient generation of Trpc4-deficient cell models for investigation of TRPC4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Trpc4 exon(s) critical for TRPC4 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 Trpc4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRPC4 CRISPR/Cas9 KO Plasmid (m) and TRPC4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trpc4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRPC4 HDR Plasmid (m) and TRPC4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trpc4 homology arms to support homology-directed repair at defined Trpc4 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.