MRP7 Double Nickase Plasmid (h): sc-406412-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MRP7 Double Nickase Plasmid (h) 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
- MRP7 Double Nickase Plasmid (h) and MRP7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ABCC10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MRP7 Double Nickase Plasmid (h) | sc-406412-NIC | 20 µg | $410.00 |
ABCC10 encodes the human ATP-binding cassette transporter MRP7 (ABCC10), a plasma membrane efflux pump that uses ATP hydrolysis to export a broad range of xenobiotics and endogenous metabolites. MRP7 activity contributes to cellular detoxification and influences intracellular drug disposition, intersecting with pathways governing membrane transport, lipid handling, and cellular stress responses. Dysregulated ABCC10/MRP7 expression or function has been linked to altered chemoresistance phenotypes in cancer models and to variation in pharmacokinetic traits, making it relevant for studies of transporter biology and drug–transporter interactions. As a member of the ABCC subfamily, MRP7 also provides a tractable system for dissecting how ABC transporters shape barrier functions and tissue-specific distribution of small molecules.
MRP7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ABCC10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ABCC10. 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 ABCC10 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 ABCC10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.