TLR7 Double Nickase Plasmid (m): sc-431302-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR7 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
- TLR7 Double Nickase Plasmid (m) and TLR7 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tlr7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TLR7 Double Nickase Plasmid (m) | sc-431302-NIC | 20 µg | $410.00 | |||
TLR7 Double Nickase Plasmid (m2) | sc-431302-NIC-2 | 20 µg | $410.00 |
Mouse Toll-like receptor 7 (Tlr7; TLR7) is an endosomal pattern-recognition receptor that detects single-stranded RNA and synthetic imidazoquinoline ligands to initiate innate immune signaling. Upon activation, TLR7 engages MYD88-dependent pathways that drive NF-κB and IRF7 activation, promoting proinflammatory cytokine production and type I interferon responses. TLR7 activity shapes antiviral defense and influences B cell and dendritic cell function, linking nucleic acid sensing to adaptive immunity. Dysregulated TLR7 signaling has been implicated in inflammation and autoimmunity, making it a relevant target for mechanistic studies in immune homeostasis and disease models.
TLR7 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tlr7 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tlr7. 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 Tlr7 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 Tlr7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.