SELENBP1 Double Nickase Plasmid (m): sc-422870-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SELENBP1 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
- SELENBP1 Double Nickase Plasmid (m) and SELENBP1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Selenbp1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SELENBP1 Double Nickase Plasmid (m) | sc-422870-NIC | 20 µg | $410.00 | |||
SELENBP1 Double Nickase Plasmid (m2) | sc-422870-NIC-2 | 20 µg | $410.00 |
Selenbp1 encodes selenium-binding protein 1 (SELENBP1), a cytosolic protein implicated in selenium-dependent cellular metabolism and redox homeostasis. In mouse tissues it is linked to regulation of oxidative stress responses and protein quality control processes, with reported connections to cellular differentiation and metabolic state. Altered SELENBP1 expression has been associated with inflammatory and metabolic phenotypes and is frequently studied as a marker of cellular stress adaptation and tumor-related transcriptional reprogramming. These features make Selenbp1 a useful node for investigating selenium biology, redox-sensitive signaling, and context-dependent changes in cellular metabolism.
SELENBP1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Selenbp1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Selenbp1. 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 Selenbp1 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 Selenbp1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.