TRPM5 CRISPR/Cas9 KO Plasmid (h): sc-403223
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRPM5 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 TRPM5 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 | |
TRPM5 CRISPR/Cas9 KO Plasmid (h) | sc-403223 | 20 µg | $397.00 |
Overview
TRPM5 (transient receptor potential cation channel subfamily M member 5) is a Ca2+-activated, monovalent cation channel that depolarizes the plasma membrane in response to intracellular calcium signals. It functions downstream of phospholipase C signaling and IP3-mediated Ca2+ release, shaping stimulus-evoked electrical activity and signal amplification in chemosensory and secretory cell types. TRPM5 activity is linked to GPCR-driven pathways involved in taste transduction and other calcium-dependent cellular responses, influencing excitability and downstream transcriptional programs. Dysregulated TRPM5 expression or function has been associated with altered sensory signaling and has been investigated in the context of cancer cell behavior and metabolic signaling phenotypes.
TRPM5 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TRPM5 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TRPM5 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 TRPM5 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 TRPM5 protein expression.
This CRISPR knockout system enables efficient generation of TRPM5-deficient cell models for investigation of TRPM5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TRPM5 exon(s) critical for TRPM5 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 TRPM5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRPM5 CRISPR/Cas9 KO Plasmid (h) and TRPM5 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TRPM5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRPM5 HDR Plasmid (h) and TRPM5 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TRPM5 homology arms to support homology-directed repair at defined TRPM5 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.