MYEF2 Double Nickase Plasmid (h): sc-405299-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MYEF2 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
- MYEF2 Double Nickase Plasmid (h) and MYEF2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MYEF2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MYEF2 Double Nickase Plasmid (h) | sc-405299-NIC | 20 µg | $410.00 |
MYEF2 (myelin expression factor 2) encodes a DNA-binding transcriptional regulator that recognizes the MEF2 motif and modulates gene expression programs linked to cellular differentiation and lineage-specific transcription. In human cells, MYEF2 has been studied in the context of transcriptional control mechanisms that influence myelin-related gene regulation and broader RNA polymerase II–dependent regulatory networks. By shaping promoter and enhancer activity, MYEF2 can affect downstream pathways involved in cell identity, maturation, and response to developmental cues. Altered regulation of transcription factors such as MYEF2 is relevant to research on neurological biology and disease-associated dysregulation of gene expression without implying clinical outcomes.
MYEF2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MYEF2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MYEF2. 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 MYEF2 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 MYEF2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.