TRPM4 Double Nickase Plasmid (m): sc-427134-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRPM4 Double Nickase Plasmid (m) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- TRPM4 Double Nickase Plasmid (m) and TRPM4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Trpm4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRPM4 Double Nickase Plasmid (m) | sc-427134-NIC | 20 µg | $410.00 |
Trpm4 encodes TRPM4, a Ca2+-activated, monovalent-selective cation channel that conducts Na+ to depolarize the plasma membrane without directly transporting Ca2+. By shaping membrane potential, TRPM4 modulates Ca2+ entry indirectly and influences excitation–contraction coupling, immune cell activation, and secretory signaling downstream of PLC/IP3-dependent Ca2+ release. In mouse tissues, TRPM4 activity has been linked to regulation of cardiac conduction and contractility, smooth muscle tone, and inflammatory signaling programs. Altered TRPM4 function is therefore studied in models of arrhythmia-related electrophysiology, vascular dysfunction, and immune-mediated pathology.
TRPM4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Trpm4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Trpm4. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt Trpm4 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of Trpm4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.