JunD Double Nickase Plasmid (h): sc-400713-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- JunD 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
- JunD Double Nickase Plasmid (h) and JunD Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting JUND. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: JunD Antibody (D-9): sc-271938
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
JunD Double Nickase Plasmid (h) | sc-400713-NIC | 20 µg | $410.00 | |||
JunD Double Nickase Plasmid (h2) | sc-400713-NIC-2 | 20 µg | $410.00 |
JUND encodes JunD, an AP-1 family transcription factor that dimerizes with JUN and FOS proteins to regulate stimulus-dependent gene expression programs. JunD integrates signals from MAPK/ERK and JNK pathways to control proliferation, differentiation, oxidative stress responses, and apoptosis through transcriptional modulation of cell cycle and inflammatory genes. Altered AP-1 activity involving JunD has been implicated in oncogenic transformation, fibrosis, and chronic inflammatory states, making JUND a relevant node for dissecting context-specific transcriptional networks. In human cells, JunD also contributes to chromatin-associated regulatory complexes that tune enhancer activity and stress-adaptive transcription.
JunD Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the JUND locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within JUND. 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 JUND 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 JUND-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.