Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
TLR4 Double Nickase Plasmid (m): sc-423419-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR4 Double Nickase Plasmid (m) 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
- TLR4 Double Nickase Plasmid (m) and TLR4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tlr4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TLR4 Antibody (25): sc-293072
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TLR4 Double Nickase Plasmid (m) | sc-423419-NIC | 20 µg | $410.00 |
Mouse Tlr4 encodes Toll-like receptor 4 (TLR4), a pattern-recognition receptor that detects lipopolysaccharide and other damage-associated ligands to initiate innate immune signaling. Upon activation, TLR4 engages MyD88- and TRIF-dependent pathways, driving NF-κB and IRF3 transcriptional programs that regulate pro-inflammatory cytokines, type I interferon responses, and costimulatory signals. TLR4 signaling influences macrophage and dendritic cell activation, cytokine secretion, and leukocyte recruitment, linking pathogen sensing to tissue inflammation. Dysregulated TLR4 activity is widely studied in models of sepsis-like inflammation, metabolic inflammation, atherosclerosis, and neuroinflammatory processes.
TLR4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tlr4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tlr4. 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 Tlr4 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 Tlr4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.