ERdj4 Double Nickase Plasmid (h): sc-410882-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ERdj4 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
- ERdj4 Double Nickase Plasmid (h) and ERdj4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DNAJB9. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ERdj4 Double Nickase Plasmid (h) | sc-410882-NIC | 20 µg | $410.00 | |||
ERdj4 Double Nickase Plasmid (h2) | sc-410882-NIC-2 | 20 µg | $410.00 |
Human DNAJB9 encodes ERdj4, an endoplasmic reticulum (ER) lumenal Hsp40/DnaJ co-chaperone that partners with BiP/HSPA5 to promote protein folding and enforce ER quality control. ERdj4 participates in the unfolded protein response (UPR) and ER-associated degradation (ERAD), supporting proteostasis by recognizing misfolded client proteins and facilitating their processing during ER stress. Through these pathways, DNAJB9 helps regulate secretory protein maturation and cellular adaptation to proteotoxic stress, processes implicated in disorders characterized by aberrant protein aggregation and chronic UPR signaling. Altered DNAJB9/ERdj4 expression has been reported in contexts of cellular stress and has been used as a molecular readout in studies linking ER proteostasis to inflammatory and metabolic dysfunction.
ERdj4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DNAJB9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DNAJB9. 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 DNAJB9 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 DNAJB9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.