RECS1 Double Nickase Plasmid (m): sc-427482-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RECS1 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
- RECS1 Double Nickase Plasmid (m) and RECS1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tmbim1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RECS1 Double Nickase Plasmid (m) | sc-427482-NIC | 20 µg | $410.00 |
Mouse Tmbim1 encodes RECS1, a conserved transmembrane regulator of cell survival linked to endoplasmic reticulum and mitochondrial membrane homeostasis. RECS1 is associated with modulation of apoptotic susceptibility and stress-adaptive signaling, including pathways connected to calcium handling, unfolded protein response, and autophagy-lysosome turnover. Through these processes, Tmbim1 has been studied in contexts where dysregulated proteostasis and programmed cell death contribute to tissue injury and degenerative phenotypes. RECS1 biology is therefore relevant for mechanistic work on stress signaling networks, survival checkpoints, and membrane-associated regulation of apoptosis in mouse models.
RECS1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tmbim1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tmbim1. 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 Tmbim1 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 Tmbim1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.