TIRAP Double Nickase Plasmid (m): sc-431178-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TIRAP 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
- TIRAP Double Nickase Plasmid (m) and TIRAP Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tirap. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TIRAP Double Nickase Plasmid (m) | sc-431178-NIC | 20 µg | $410.00 | |||
TIRAP Double Nickase Plasmid (m2) | sc-431178-NIC-2 | 20 µg | $410.00 |
Mouse Tirap encodes TIRAP (also known as Mal), an adaptor that couples Toll-like receptors and interleukin-1 receptor family signaling to downstream activation of NF-κB and MAPK pathways. TIRAP helps recruit MYD88 to receptors such as TLR2 and TLR4 at the plasma membrane through phosphoinositide-dependent localization, shaping early innate immune signal transduction. By modulating cytokine and chemokine induction, Tirap influences macrophage and dendritic cell responses, inflammatory polarization, and host–microbe interactions. Dysregulated TIRAP-dependent signaling is studied in the context of aberrant inflammation and immune-mediated pathology, making it a useful node for dissecting PRR signaling networks.
TIRAP Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tirap locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tirap. 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 Tirap 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 Tirap-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.