METTL11A Double Nickase Plasmid (h): sc-412015-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- METTL11A 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
- METTL11A Double Nickase Plasmid (h) and METTL11A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting NTMT1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
METTL11A Double Nickase Plasmid (h) | sc-412015-NIC | 20 µg | $410.00 | |||
METTL11A Double Nickase Plasmid (h2) | sc-412015-NIC-2 | 20 µg | $410.00 |
NTMT1 encodes the human N-terminal methyltransferase METTL11A, a SAM-dependent enzyme that catalyzes α-N-methylation of protein N-termini after initiator methionine removal. This N-terminal methylation can influence protein–protein interactions, stability, and subcellular localization, linking METTL11A to proteostasis and regulation of signaling and nuclear processes. METTL11A activity intersects with broader methylation-dependent regulatory networks, including chromatin-associated and stress-response pathways via modulation of methylated substrates. Dysregulated N-terminal methylation has been associated with altered cell growth and differentiation programs, making NTMT1 a useful locus for mechanistic studies of methylation-driven phenotypes and pathway rewiring in disease-relevant models.
METTL11A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the NTMT1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within NTMT1. 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 NTMT1 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 NTMT1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.