FTSJD2 Double Nickase Plasmid (h): sc-409236-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FTSJD2 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
- FTSJD2 Double Nickase Plasmid (h) and FTSJD2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CMTR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FTSJD2 Double Nickase Plasmid (h) | sc-409236-NIC | 20 µg | $410.00 | |||
FTSJD2 Double Nickase Plasmid (h2) | sc-409236-NIC-2 | 20 µg | $410.00 |
CMTR1 (also known as FTSJD2) encodes a cap-specific 2′-O-ribose methyltransferase that catalyzes formation of the mRNA cap1 structure on RNA polymerase II transcripts. This modification supports efficient pre-mRNA processing, translation, and transcript stability, and helps shape innate immune discrimination between self and non-self RNA through interferon-linked RNA sensing pathways. CMTR1 activity is integrated with broader RNA metabolism programs that influence gene expression homeostasis in human cells. Dysregulation of cap methylation machinery, including CMTR1-dependent steps, is studied in the context of altered interferon signaling, antiviral responses, and cancer-associated transcriptional rewiring.
FTSJD2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CMTR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CMTR1. 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 CMTR1 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 CMTR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.