SEC16A Double Nickase Plasmid (m): sc-432718-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEC16A 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
- SEC16A Double Nickase Plasmid (m) and SEC16A Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sec16a. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SEC16A Double Nickase Plasmid (m) | sc-432718-NIC | 20 µg | $410.00 | |||
SEC16A Double Nickase Plasmid (m2) | sc-432718-NIC-2 | 20 µg | $410.00 |
Sec16a encodes SEC16A, a core scaffold of endoplasmic reticulum exit sites that organizes COPII coat assembly to initiate ER-to-Golgi transport. By coordinating the recruitment and dynamics of SEC23/SEC24 and SEC13/SEC31, SEC16A regulates secretory pathway flux and the biogenesis of transport carriers that support membrane trafficking, organelle homeostasis, and proteostasis. Altered early secretory trafficking can perturb lipid metabolism, extracellular matrix secretion, and receptor presentation, processes relevant to stress adaptation and cell-state transitions. SEC16A is therefore studied in pathways linking ER organization to autophagy, unfolded protein response signaling, and trafficking-dependent regulation of cell growth and differentiation in mouse models.
SEC16A Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sec16a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sec16a. 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 Sec16a 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 Sec16a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.