MFSD2 Double Nickase Plasmid (m): sc-429366-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MFSD2 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
- MFSD2 Double Nickase Plasmid (m) and MFSD2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mfsd2a. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MFSD2 Double Nickase Plasmid (m) | sc-429366-NIC | 20 µg | $410.00 |
Mfsd2a encodes MFSD2, a multipass membrane transporter of the major facilitator superfamily that is highly enriched in endothelial barriers and contributes to lipid and nutrient transport across specialized vascular interfaces. In mouse, MFSD2A is best known for regulating transcytosis in brain microvascular endothelium, supporting blood–brain barrier integrity and influencing CNS homeostasis. Through its role in membrane transport and vesicular trafficking control, MFSD2A impacts lipid metabolism pathways and cellular barrier functions relevant to neurodevelopment and neuroinflammation models. Altered MFSD2A activity has been associated with barrier dysfunction phenotypes and neurological disease mechanisms, making it a useful target for studying endothelial transport biology and CNS-relevant metabolic regulation.
MFSD2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mfsd2a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mfsd2a. 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 Mfsd2a 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 Mfsd2a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.