TIS11D Double Nickase Plasmid (h): sc-405406-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TIS11D 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
- TIS11D Double Nickase Plasmid (h) and TIS11D Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ZFP36L2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TIS11D Antibody (A-3): sc-365908
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TIS11D Double Nickase Plasmid (h) | sc-405406-NIC | 20 µg | $410.00 |
Human ZFP36L2 encodes the RNA-binding protein TIS11D, a CCCH-type zinc finger factor that recognizes AU-rich elements in 3′ UTRs to promote mRNA deadenylation and decay. Through regulation of transcript stability, TIS11D shapes gene expression programs linked to lymphocyte development, activation, and differentiation, intersecting with MAPK- and NF-κB-associated inflammatory signaling and broader post-transcriptional control networks. ZFP36L2 has been implicated in immune homeostasis and oncogenic phenotypes in hematologic contexts, where altered RNA turnover can influence proliferation, apoptosis, and lineage commitment. These features make ZFP36L2 a useful node for dissecting RNA decay pathways and immune-related transcriptional outputs in human cell models.
TIS11D Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ZFP36L2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ZFP36L2. 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 ZFP36L2 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 ZFP36L2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.