CD27L Double Nickase Plasmid (h): sc-402625-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD27L 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
- CD27L Double Nickase Plasmid (h) and CD27L Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CD70. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CD27L Antibody (G-7): sc-365539
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD27L Double Nickase Plasmid (h) | sc-402625-NIC | 20 µg | $410.00 | |||
CD27L Double Nickase Plasmid (h2) | sc-402625-NIC-2 | 20 µg | $410.00 |
CD70, also known as CD27 ligand (CD27L), is a type II transmembrane member of the TNF superfamily expressed primarily on activated antigen-presenting cells and subsets of lymphocytes. By engaging CD27 on T and B cells, CD70 delivers co-stimulatory signals that shape lymphocyte activation, proliferation, survival, and differentiation, supporting germinal center responses and cytotoxic effector development. CD70–CD27 signaling interfaces with NF-κB and MAPK-dependent transcriptional programs and helps regulate immune homeostasis during inflammation. Dysregulated CD70 expression has been associated with altered immune activation states and is frequently investigated in contexts of tumor immune microenvironments and chronic inflammatory disease biology.
CD27L Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CD70 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CD70. 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 CD70 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 CD70-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.