CD8-β Double Nickase Plasmid (h): sc-400950-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD8-β 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
- CD8-β Double Nickase Plasmid (h) and CD8-β Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CD8B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CD8-β Antibody (F-5): sc-25277
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD8-β Double Nickase Plasmid (h) | sc-400950-NIC | 20 µg | $410.00 | |||
CD8-β Double Nickase Plasmid (h2) | sc-400950-NIC-2 | 20 µg | $410.00 |
CD8B encodes the CD8-β chain, a transmembrane glycoprotein that pairs with CD8-α to form the CD8 co-receptor on cytotoxic T lymphocytes. By binding MHC class I molecules, CD8 enhances TCR sensitivity and recruits Src-family kinase LCK to amplify downstream signaling cascades that shape activation, effector differentiation, and immune synapse formation. CD8B expression and CD8 co-receptor composition influence antigen-specific cytotoxic responses, T cell exhaustion programs, and immune surveillance dynamics. Altered CD8 lineage function is relevant to studies of chronic viral infection, tumor immunology, and immune dysregulation, where CD8 signaling thresholds impact phenotype and function.
CD8-β Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CD8B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CD8B. 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 CD8B 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 CD8B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.