Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
JNK2 Double Nickase Plasmid (h): sc-400115-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- JNK2 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
- JNK2 Double Nickase Plasmid (h) and JNK2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MAPK9. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: JNK2 Antibody (A-7): sc-271133
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
JNK2 Double Nickase Plasmid (h) | sc-400115-NIC | 20 µg | $410.00 | |||
JNK2 Double Nickase Plasmid (h2) | sc-400115-NIC-2 | 20 µg | $410.00 |
MAPK9 encodes c-Jun N-terminal kinase 2 (JNK2), a stress-activated MAP kinase that phosphorylates transcription factors such as c-JUN and ATF2 to coordinate inflammatory signaling, apoptosis, and cell-cycle control. JNK2 functions downstream of MAP3Ks and MAP2Ks in the JNK/MAPK cascade, integrating cues from cytokines, oxidative stress, ER stress, and genotoxic damage to regulate context-dependent transcriptional programs. Through modulation of AP-1 activity and cross-talk with NF-κB and p53-associated pathways, MAPK9 influences immune responses, neuronal signaling, and tissue remodeling. Dysregulated JNK2 signaling has been implicated in cancer-associated stress adaptation, neurodegenerative processes, and metabolic and inflammatory phenotypes, making MAPK9 a common target for mechanistic pathway studies.
JNK2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MAPK9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MAPK9. 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 MAPK9 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 MAPK9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.