RelB Double Nickase Plasmid (h): sc-400371-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RelB 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
- RelB Double Nickase Plasmid (h) and RelB Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RELB. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RelB Antibody (D-4): sc-48366
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RelB Double Nickase Plasmid (h) | sc-400371-NIC | 20 µg | $410.00 | |||
RelB Double Nickase Plasmid (h2) | sc-400371-NIC-2 | 20 µg | $410.00 |
RELB encodes RelB, a transcription factor in the NF-κB family that predominantly functions in the non-canonical NF-κB pathway through heterodimerization with p52 (NFKB2). RelB regulates gene programs involved in dendritic cell maturation, lymphoid organogenesis, B-cell survival, and inflammatory signaling, integrating inputs from receptors such as CD40, BAFFR, and LTβR. By shaping cytokine and chemokine expression as well as antigen presentation pathways, RelB influences innate and adaptive immune responses. Dysregulated RELB activity has been associated with immune dysfunction and inflammatory phenotypes, and altered NF-κB pathway balance is frequently studied in the context of tumor microenvironment signaling and hematologic malignancy biology.
RelB Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RELB locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RELB. 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 RELB 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 RELB-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.