TRPC5 CRISPR/Cas9 KO Plasmid (m): sc-423516
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRPC5 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 TRPC5 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: TRPC5 Antibody (1C8): sc-293259
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRPC5 CRISPR/Cas9 KO Plasmid (m) | sc-423516 | 20 µg | $397.00 |
Overview
Trpc5 encodes TRPC5, a non-selective cation channel of the transient receptor potential canonical family that mediates Ca²⁺ influx in response to receptor-operated and lipid-dependent signaling. TRPC5 participates in PLC-dependent pathways downstream of GPCRs and receptor tyrosine kinases, shaping membrane excitability, intracellular calcium homeostasis, and calcium-dependent transcriptional programs. In mouse systems, TRPC5 is broadly studied in neurons and vascular/endothelial contexts where it influences synaptic function, neurite dynamics, mechanosensitive responses, and redox-sensitive signaling. Dysregulated TRPC5 activity has been linked to processes relevant to pain signaling, anxiety-like behaviors, vascular remodeling, and kidney injury mechanisms, supporting its use in models of neurobiology, cardiovascular biology, and renal pathophysiology.
TRPC5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trpc5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trpc5 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 Trpc5 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 TRPC5 protein expression.
This CRISPR knockout system enables efficient generation of Trpc5-deficient cell models for investigation of TRPC5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Trpc5 exon(s) critical for TRPC5 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 Trpc5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRPC5 CRISPR/Cas9 KO Plasmid (m) and TRPC5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trpc5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRPC5 HDR Plasmid (m) and TRPC5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trpc5 homology arms to support homology-directed repair at defined Trpc5 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.