TLR2 Double Nickase Plasmid (h): sc-400267-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR2 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
- TLR2 Double Nickase Plasmid (h) and TLR2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TLR2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TLR2 Antibody (TL2.1): sc-21759
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TLR2 Double Nickase Plasmid (h) | sc-400267-NIC | 20 µg | $410.00 | |||
TLR2 Double Nickase Plasmid (h2) | sc-400267-NIC-2 | 20 µg | $410.00 |
TLR2 encodes Toll-like receptor 2, a plasma membrane pattern-recognition receptor that detects bacterial lipoproteins and other microbial ligands, frequently via heterodimerization with TLR1 or TLR6. Upon activation, TLR2 signals through MYD88- and TIRAP-dependent pathways to induce NF-κB and MAPK cascades, driving transcription of pro-inflammatory cytokines and chemokines and shaping innate-to-adaptive immune crosstalk. TLR2 activity also interfaces with phagocytosis, autophagy, and inflammasome-related programs, influencing antimicrobial responses and tissue homeostasis. Dysregulated TLR2 signaling has been implicated in chronic inflammatory states and infection-associated pathology, making it a widely studied node in host–microbe and sterile inflammation research.
TLR2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TLR2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TLR2. 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 TLR2 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 TLR2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.