YTHDF2 Double Nickase Plasmid (h2): sc-416408-NIC-2
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- YTHDF2 Double Nickase Plasmid (h2) 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
- YTHDF2 Double Nickase Plasmid (h2) and YTHDF2 Double Nickase Plasmid (h22) encode distinct paired gRNA designs targeting YTHDF2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
YTHDF2 Double Nickase Plasmid (h2) | sc-416408-NIC-2 | 20 µg | $410.00 |
Human YTHDF2 encodes an m6A reader protein that selectively binds N6-methyladenosine–modified mRNAs and promotes their decay, thereby shaping transcript stability and translation output. Through recruitment of deadenylation and RNA turnover machinery, YTHDF2 contributes to post-transcriptional regulation in processes including cell fate decisions, stress responses, and immune signaling. Dysregulated YTHDF2 activity has been linked to altered epitranscriptomic control in cancer biology, inflammation, and viral infection models, where changes in mRNA clearance can remodel gene expression programs. Genome editing of YTHDF2 supports mechanistic studies of m6A-dependent RNA metabolism, mapping of reader–target networks, and functional interrogation of pathways governing proliferation, differentiation, and innate immune regulation.
YTHDF2 Double Nickase Plasmid (h2) consists of a matched pair of plasmids engineered for high-specificity editing of the YTHDF2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within YTHDF2. 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 YTHDF2 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 YTHDF2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.