c-Jun Double Nickase Plasmid (h): sc-400077-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- c-Jun 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
- c-Jun Double Nickase Plasmid (h) and c-Jun Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting JUN. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: p-c-Jun Antibody (KM-1): sc-822
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
c-Jun Double Nickase Plasmid (h) | sc-400077-NIC | 20 µg | $410.00 | |||
c-Jun Double Nickase Plasmid (h2) | sc-400077-NIC-2 | 20 µg | $410.00 |
JUN encodes c-Jun, a leucine-zipper transcription factor that heterodimerizes with FOS proteins to form the AP-1 complex and regulate stimulus-responsive gene expression. c-Jun integrates signals from MAPK pathways, including JNK and ERK cascades, to control proliferation, differentiation, apoptosis, and cellular stress responses. Through AP-1–dependent transcriptional programs, c-Jun modulates inflammatory signaling, extracellular matrix remodeling, and cell-cycle progression. Dysregulated JUN/AP-1 activity is frequently associated with oncogenic transformation, invasion, and therapy resistance, and is also implicated in pathological inflammatory and fibrotic processes.
c-Jun Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the JUN locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within JUN. 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 JUN 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 JUN-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.