DOM3Z Double Nickase Plasmid (h): sc-409469-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DOM3Z 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
- DOM3Z Double Nickase Plasmid (h) and DOM3Z Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DXO. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: DOM3Z Antibody (D-9): sc-393167
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DOM3Z Double Nickase Plasmid (h) | sc-409469-NIC | 20 µg | $410.00 | |||
DOM3Z Double Nickase Plasmid (h2) | sc-409469-NIC-2 | 20 µg | $410.00 |
DXO (also known as DOM3Z) encodes a metallo-β-lactamase–like RNA decapping and exonuclease that contributes to cytoplasmic RNA quality control. DOM3Z participates in surveillance pathways that remove aberrantly capped or incompletely processed RNAs, thereby shaping mRNA stability and coupling decapping to 5′→3′ RNA decay. By influencing turnover of defective transcripts and decay intermediates, DXO helps maintain transcriptome fidelity during cellular stress responses and RNA processing. Dysregulation of RNA decay and surveillance networks is frequently linked to altered gene-expression programs observed in cancer and neurodegenerative and inflammatory contexts, making DXO a relevant target for mechanistic studies.
DOM3Z Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DXO locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DXO. 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 DXO 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 DXO-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.