MsrB2 Double Nickase Plasmid (h): sc-411635-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MsrB2 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
- MsrB2 Double Nickase Plasmid (h) and MsrB2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MSRB2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MsrB2 Antibody (B-12): sc-515088
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MsrB2 Double Nickase Plasmid (h) | sc-411635-NIC | 20 µg | $410.00 | |||
MsrB2 Double Nickase Plasmid (h2) | sc-411635-NIC-2 | 20 µg | $410.00 |
MSRB2 encodes methionine sulfoxide reductase B2 (MsrB2), a mitochondrial enzyme that catalyzes stereospecific reduction of methionine-R-sulfoxide residues back to methionine, helping maintain protein function under oxidative stress. By repairing oxidized methionine and supporting redox homeostasis, MsrB2 contributes to mitochondrial quality control, reactive oxygen species handling, and proteostasis pathways that influence cell survival and metabolism. Altered MSRB2 activity or expression has been linked to oxidative damage phenotypes relevant to neurodegeneration, metabolic dysregulation, and cancer-associated stress adaptation. Accordingly, MSRB2 is frequently studied in contexts of mitochondrial dysfunction, redox signaling, and stress-responsive gene networks.
MsrB2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MSRB2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MSRB2. 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 MSRB2 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 MSRB2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.