METTL14 Double Nickase Plasmid (h): sc-406936-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- METTL14 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
- METTL14 Double Nickase Plasmid (h) and METTL14 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting METTL14. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
METTL14 Double Nickase Plasmid (h) | sc-406936-NIC | 20 µg | $410.00 | |||
METTL14 Double Nickase Plasmid (h2) | sc-406936-NIC-2 | 20 µg | $410.00 |
METTL14 encodes a core component of the N6-methyladenosine (m6A) RNA methyltransferase “writer” complex, partnering with METTL3 and adaptor proteins such as WTAP to deposit m6A marks on mRNA and other RNAs. These epitranscriptomic modifications regulate RNA splicing, nuclear export, stability, and translation, thereby shaping gene expression programs controlling cell fate decisions, proliferation, and stress responses. METTL14-dependent m6A signaling intersects with pathways governing DNA damage responses, stemness, and innate immune regulation through altered transcript turnover and translational output. Dysregulated METTL14 activity or expression has been linked to aberrant epigenetic-like control of oncogenic and developmental networks, making it a common target in mechanistic studies of tumor biology and differentiation.
METTL14 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the METTL14 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within METTL14. 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 METTL14 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 METTL14-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.