Derlin-1 Double Nickase Plasmid (m): sc-426756-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Derlin-1 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
- Derlin-1 Double Nickase Plasmid (m) and Derlin-1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Derl1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Derlin-1 Antibody (1B9): sc-293385
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Derlin-1 Double Nickase Plasmid (m) | sc-426756-NIC | 20 µg | $410.00 |
Derl1 encodes Derlin-1, an endoplasmic reticulum (ER) membrane component of the ER-associated degradation (ERAD) machinery that helps recognize and retrotranslocate misfolded luminal and membrane proteins for ubiquitin–proteasome turnover. Derlin-1 functions within proteostasis networks linked to the unfolded protein response (UPR), coordinating with ubiquitination factors and ATPase-driven extraction complexes to maintain ER homeostasis. Disruption of DERL1-dependent quality control can elevate ER stress signaling and alter secretory pathway function, connecting this pathway to cell survival decisions under proteotoxic stress. In mouse systems, Derl1 is frequently studied in contexts where ERAD and UPR remodeling influence immune function, metabolic homeostasis, and neurobiology-relevant proteostasis phenotypes.
Derlin-1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Derl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Derl1. 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 Derl1 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 Derl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.