MyD88 Double Nickase Plasmid (m): sc-421774-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MyD88 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
- MyD88 Double Nickase Plasmid (m) and MyD88 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Myd88. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MyD88 Antibody (E-11): sc-74532
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MyD88 Double Nickase Plasmid (m) | sc-421774-NIC | 20 µg | $410.00 | |||
MyD88 Double Nickase Plasmid (m2) | sc-421774-NIC-2 | 20 µg | $410.00 |
Mouse Myd88 encodes myeloid differentiation primary response protein 88 (MyD88), an essential adaptor for most Toll-like receptors and interleukin-1 receptor family members that couples receptor engagement to IRAK–TRAF6 signaling, NF-κB activation, and MAPK-driven inflammatory gene expression. MyD88-dependent signaling coordinates innate immune cell activation, cytokine production, and antimicrobial responses while shaping downstream adaptive immunity. Dysregulated MyD88 pathways are widely used to model aberrant inflammatory signaling in infection biology and inflammatory disease mechanisms, and to study how innate immune cues influence tissue homeostasis and tumor–immune interactions.
MyD88 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Myd88 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Myd88. 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 Myd88 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 Myd88-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.