hDcp2 Double Nickase Plasmid (h): sc-418511-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- hDcp2 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
- hDcp2 Double Nickase Plasmid (h) and hDcp2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DCP2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
hDcp2 Double Nickase Plasmid (h) | sc-418511-NIC | 20 µg | $410.00 |
DCP2 encodes the human decapping enzyme hDcp2, a core component of cytoplasmic mRNA turnover that catalyzes removal of the 5′ m7G cap to initiate 5′→3′ decay by XRN1. hDcp2 functions within mRNA decapping complexes and P-bodies, integrating signals from translation, stress responses, and RNA quality control to shape transcriptome dynamics. Through control of mRNA stability and processing, DCP2 influences pathways such as nonsense-mediated decay, miRNA-mediated repression, and stress granule/P-body interchange. Dysregulated decapping activity has been linked in the literature to altered RNA homeostasis and disease-relevant phenotypes, including neurodevelopmental and cancer-associated gene expression programs.
hDcp2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DCP2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DCP2. 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 DCP2 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 DCP2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.