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.
RELA/NFκB p65 Double Nickase Plasmid (h): sc-400004-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RELA/NFκB p65 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
- RELA/NFκB p65 Double Nickase Plasmid (h) and RELA/NFκB p65 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RELA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RELA/NFκB p65 Antibody (F-6): sc-8008
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RELA/NFκB p65 Double Nickase Plasmid (h) | sc-400004-NIC | 20 µg | $410.00 | |||
RELA/NFκB p65 Double Nickase Plasmid (h2) | sc-400004-NIC-2 | 20 µg | $410.00 |
RELA encodes the NFκB p65 subunit, a central transcription factor that forms heterodimers (commonly with NFKB1/p50) to regulate inducible gene programs controlling inflammation, innate and adaptive immune responses, cell survival, and stress signaling. In canonical NFκB signaling, upstream cues such as TNF, IL-1, and pattern-recognition receptor activation converge on IKK-mediated IκB phosphorylation and degradation, enabling p65 nuclear translocation and transcriptional activation. RELA activity is further shaped by post-translational modifications and cross-talk with MAPK, JAK/STAT, and interferon pathways, influencing cytokine production, apoptosis resistance, and cellular differentiation. Dysregulated NFκB/RELA signaling is frequently implicated in chronic inflammatory states and oncogenic processes, including altered tumor microenvironment signaling and survival pathway engagement.
RELA/NFκB p65 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RELA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RELA. 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 RELA 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 RELA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.