MIF Double Nickase Plasmid (m): sc-421649-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MIF 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
- MIF Double Nickase Plasmid (m) and MIF Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mif. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MIF Antibody (D-2): sc-271631
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MIF Double Nickase Plasmid (m) | sc-421649-NIC | 20 µg | $410.00 | |||
MIF Double Nickase Plasmid (m2) | sc-421649-NIC-2 | 20 µg | $410.00 |
Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine encoded by the mouse Mif gene that regulates innate and adaptive immune responses, leukocyte trafficking, and stress signaling. MIF engages CD74/CD44 and chemokine receptors such as CXCR2/CXCR4 to coordinate MAPK and NF-κB pathway activity, shaping cytokine production and cell survival programs. It also interfaces with glucocorticoid counter-regulation and redox control, linking inflammatory cues to metabolic and proliferative outputs. Dysregulated MIF signaling has been implicated in chronic inflammation, autoimmunity, and tumor-associated immune remodeling, making Mif a common target for mechanistic studies in immunology and cancer biology.
MIF Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mif locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mif. 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 Mif 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 Mif-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.