METT11D1 Double Nickase Plasmid (h): sc-413022-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- METT11D1 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
- METT11D1 Double Nickase Plasmid (h) and METT11D1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting METTL17. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
METT11D1 Double Nickase Plasmid (h) | sc-413022-NIC | 20 µg | $410.00 |
Human METTL17 (also known as METT11D1) encodes a putative S-adenosylmethionine–dependent methyltransferase that has been linked to mitochondrial gene expression and maintenance of oxidative phosphorylation capacity. Evidence from functional genomics supports a role in regulating mitochondrial translation and/or ribosome-associated processes that influence respiratory chain assembly, ATP production, and cellular redox balance. Perturbation of METTL17 is therefore relevant to pathways controlling mitochondrial proteostasis, energy metabolism, and stress signaling responses. Altered mitochondrial function is a recurring feature across neurodegenerative, metabolic, and cancer-related research contexts, making METTL17 a useful target for mechanistic studies of mitochondrial homeostasis.
METT11D1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the METTL17 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within METTL17. 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 METTL17 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 METTL17-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.