EXOD1 Double Nickase Plasmid (h): sc-413999-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EXOD1 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
- EXOD1 Double Nickase Plasmid (h) and EXOD1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ERI2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EXOD1 Double Nickase Plasmid (h) | sc-413999-NIC | 20 µg | $410.00 | |||
EXOD1 Double Nickase Plasmid (h2) | sc-413999-NIC-2 | 20 µg | $410.00 |
ERI2 encodes EXOD1, a 3′–5′ exonuclease implicated in RNA metabolism and nucleic acid quality control, with reported roles in processing or turnover of small RNAs and structured RNA intermediates. By modulating RNA stability and surveillance, EXOD1 is positioned within pathways that influence post-transcriptional gene regulation and cellular responses to aberrant nucleic acids. Altered regulation of RNA decay and related stress-response networks can affect genome stability, innate immune signaling, and cell-state transitions. Consequently, ERI2/EXOD1 is of interest for mechanistic studies linking RNA homeostasis to proliferative control and disease-associated transcriptional programs.
EXOD1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ERI2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ERI2. 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 ERI2 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 ERI2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.