MsrA Double Nickase Plasmid (h): sc-404424-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MsrA 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
- MsrA Double Nickase Plasmid (h) and MsrA Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MSRA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MsrA Antibody (1C8): sc-59619
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MsrA Double Nickase Plasmid (h) | sc-404424-NIC | 20 µg | $410.00 |
Human MSRA encodes methionine sulfoxide reductase A (MsrA), a cytosolic and mitochondrial repair enzyme that reduces methionine-S-sulfoxide back to methionine, reversing oxidative damage in proteins and helping preserve proteostasis. MsrA functions within cellular redox homeostasis networks that interface with thioredoxin-dependent electron transfer, mitochondrial metabolism, and antioxidant stress responses. By modulating the oxidation state of methionine residues, MSRA can influence protein folding, enzyme activity, and signaling pathways sensitive to reactive oxygen species. Altered MSRA expression or activity has been associated with oxidative stress–linked phenotypes in neurodegeneration, aging-related dysfunction, and inflammatory tissue damage, supporting its relevance in mechanistic studies of redox biology.
MsrA Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MSRA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MSRA. 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 MSRA 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 MSRA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.