MKP-4 Double Nickase Plasmid (h): sc-405872-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MKP-4 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
- MKP-4 Double Nickase Plasmid (h) and MKP-4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DUSP9. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MKP-4 Antibody (D-3): sc-137010
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MKP-4 Double Nickase Plasmid (h) | sc-405872-NIC | 20 µg | $410.00 | |||
MKP-4 Double Nickase Plasmid (h2) | sc-405872-NIC-2 | 20 µg | $410.00 |
DUSP9 encodes dual specificity phosphatase 9 (MKP-4), a MAPK phosphatase that dephosphorylates phospho-threonine and phospho-tyrosine residues on MAPKs to attenuate kinase signaling. MKP-4 is linked to regulation of ERK and p38 pathway dynamics, shaping cellular responses such as proliferation, differentiation, and stress signaling. Through feedback control of MAPK cascades, DUSP9 influences inflammatory and metabolic signaling networks and has been studied in contexts where MAPK pathway output is altered, including cancer-associated signaling states. Altered DUSP9 expression or activity is therefore relevant for dissecting MAPK-dependent phenotypes and pathway compensation mechanisms in human cells.
MKP-4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DUSP9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DUSP9. 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 DUSP9 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 DUSP9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.