MAPKAPK-2 Double Nickase Plasmid (m): sc-421557-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MAPKAPK-2 Double Nickase Plasmid (m) 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
- MAPKAPK-2 Double Nickase Plasmid (m) and MAPKAPK-2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mapkapk2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MAPKAPK-2 Antibody (A-11): sc-393609
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MAPKAPK-2 Double Nickase Plasmid (m) | sc-421557-NIC | 20 µg | $410.00 |
Mouse Mapkapk2 encodes MAPKAPK-2 (MK2), a serine/threonine kinase that acts as a key downstream effector of the p38 MAPK stress-response pathway. MK2 phosphorylates substrates such as HSPB1/Hsp27 and regulates RNA-binding proteins that control stability and translation of inflammatory cytokine mRNAs, linking stress signaling to post-transcriptional gene regulation. Through these functions it coordinates cellular responses including inflammation, innate immune signaling, apoptosis, cell-cycle checkpoints, and cytoskeletal remodeling. Dysregulated MK2 activity has been implicated in inflammatory and autoimmune phenotypes, metabolic stress responses, neuroinflammation, and tumor-associated signaling networks, making it a useful node for mechanistic pathway studies.
MAPKAPK-2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mapkapk2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mapkapk2. 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 Mapkapk2 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 Mapkapk2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.