CMTM4 Double Nickase Plasmid (m): sc-430183-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CMTM4 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
- CMTM4 Double Nickase Plasmid (m) and CMTM4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cmtm4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CMTM4 Antibody (1E8): sc-81942
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CMTM4 Double Nickase Plasmid (m) | sc-430183-NIC | 20 µg | $410.00 |
Cmtm4 encodes CMTM4, a transmembrane protein of the CKLF-like MARVEL family implicated in membrane organization and vesicular trafficking. CMTM4 participates in endosomal sorting processes that influence stability and surface availability of key immunoregulatory proteins, including PD-L1, thereby shaping cell–cell signaling and immune-related pathways. In mouse systems, CMTM4 is studied in the context of epithelial and immune cell biology where perturbations can affect proliferation, differentiation, and inflammatory responses. Dysregulated CMTM4-associated trafficking and signaling has been linked to mechanisms relevant to tumor immunology and other pathologies involving altered membrane protein turnover.
CMTM4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cmtm4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cmtm4. 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 Cmtm4 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 Cmtm4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.