TLR3 Double Nickase Plasmid (h): sc-400512-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR3 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
- TLR3 Double Nickase Plasmid (h) and TLR3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TLR3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TLR3 Antibody (TLR3.7): sc-32232
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TLR3 Double Nickase Plasmid (h) | sc-400512-NIC | 20 µg | $410.00 | |||
TLR3 Double Nickase Plasmid (h2) | sc-400512-NIC-2 | 20 µg | $410.00 |
Toll-like receptor 3 (TLR3) is an endosomal pattern-recognition receptor that detects double-stranded RNA derived from viruses or damaged cells and initiates innate immune signaling. Upon ligand engagement, TLR3 signals primarily through the TRIF adaptor to activate IRF3/IRF7-driven type I interferon responses and NF-κB-dependent inflammatory transcriptional programs. This pathway regulates cytokine and chemokine production, antigen presentation, and crosstalk with adaptive immunity, influencing antiviral defense and immune homeostasis. Altered TLR3 activity has been linked to susceptibility to viral infections and to inflammatory and autoimmune phenotypes, and it is frequently interrogated in neuroinflammation and tumor-immune microenvironment studies.
TLR3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TLR3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TLR3. 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 TLR3 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 TLR3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.