CMTM6 Double Nickase Plasmid (m): sc-426447-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CMTM6 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
- CMTM6 Double Nickase Plasmid (m) and CMTM6 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cmtm6. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CMTM6 Double Nickase Plasmid (m) | sc-426447-NIC | 20 µg | $410.00 | |||
CMTM6 Double Nickase Plasmid (m2) | sc-426447-NIC-2 | 20 µg | $410.00 |
Cmtm6 encodes CMTM6, a tetra-transmembrane MARVEL-domain protein that regulates immune checkpoint biology by stabilizing PD-L1 at the cell surface and limiting its lysosomal degradation. Through control of PD-L1 trafficking and membrane retention, CMTM6 influences cell–cell signaling, antigen-specific T cell responses, and broader inflammatory pathways in the tumor microenvironment. In mouse systems, CMTM6 is widely studied for its role in immune evasion mechanisms and its impact on interferon-driven signaling states. Dysregulated CMTM6–PD-L1 axis activity has been associated with altered immune surveillance in cancer models and with immune-mediated disease processes that depend on checkpoint regulation.
CMTM6 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cmtm6 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cmtm6. 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 Cmtm6 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 Cmtm6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.