FTSJD1 Double Nickase Plasmid (h): sc-412604-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FTSJD1 Double Nickase Plasmid (h) 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
- FTSJD1 Double Nickase Plasmid (h) and FTSJD1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CMTR2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FTSJD1 Double Nickase Plasmid (h) | sc-412604-NIC | 20 µg | $410.00 |
CMTR2 encodes FTSJD1, a cap-specific 2′-O-ribose methyltransferase that contributes to maturation of mRNA by modifying the first transcribed nucleotide to generate Cap1 structures. This epitranscriptomic mark supports proper RNA stability, translation efficiency, and discrimination of self versus non-self RNA, intersecting with innate immune sensing pathways that monitor aberrant capping and RNA processing. CMTR2 activity is therefore linked to host–virus interactions and cellular stress responses that depend on accurate transcriptome surveillance. Dysregulation of cap methylation and related RNA quality-control processes has been associated with altered inflammatory signaling and context-dependent changes in gene expression programs relevant to disease biology.
FTSJD1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CMTR2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CMTR2. 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 CMTR2 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 CMTR2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.