MLKL Double Nickase Plasmid (m): sc-428931-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MLKL 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
- MLKL Double Nickase Plasmid (m) and MLKL Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mlkl. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MLKL Double Nickase Plasmid (m) | sc-428931-NIC | 20 µg | $410.00 | |||
MLKL Double Nickase Plasmid (m2) | sc-428931-NIC-2 | 20 µg | $410.00 |
Mouse MLKL (mixed lineage kinase domain-like) is a terminal effector of necroptosis, a programmed lytic cell death pathway triggered downstream of RIPK1/RIPK3 signaling. Upon phosphorylation by RIPK3, MLKL oligomerizes, translocates to cellular membranes, and disrupts membrane integrity, linking innate immune sensing to inflammatory damage and DAMP release. MLKL-dependent necroptosis intersects with TNF receptor signaling, interferon responses, and pathogen defense programs, shaping tissue homeostasis during sterile inflammation and infection. Dysregulated MLKL activity has been implicated in inflammatory and degenerative disease models where necroptotic cell loss contributes to pathology.
MLKL Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mlkl locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mlkl. 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 Mlkl 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 Mlkl-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.