DnaJC3 Double Nickase Plasmid (m): sc-437172-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DnaJC3 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
- DnaJC3 Double Nickase Plasmid (m) and DnaJC3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Dnajc3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DnaJC3 Double Nickase Plasmid (m) | sc-437172-NIC | 20 µg | $410.00 |
Dnajc3 encodes DnaJC3, an endoplasmic reticulum–associated co-chaperone (also known as P58IPK) that helps maintain proteostasis during unfolded protein response (UPR) signaling. DnaJC3 modulates stress-responsive pathways by interacting with Hsp70 family chaperones and regulating the PERK–eIF2α arm of ER stress, thereby influencing translation control and adaptation to proteotoxic conditions. Through its roles in ER quality control and attenuation of stress kinase signaling, DnaJC3 is relevant to research on secretory cell function, inflammation, and metabolic stress. Altered ER stress handling linked to DnaJC3 activity is frequently explored in contexts such as pancreatic β-cell homeostasis, neurodegeneration-associated proteostasis imbalance, and broader stress-response phenotypes in mouse models.
DnaJC3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Dnajc3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Dnajc3. 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 Dnajc3 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 Dnajc3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.