ERV3 Double Nickase Plasmid (h): sc-410773-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ERV3 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
- ERV3 Double Nickase Plasmid (h) and ERV3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ERV3-1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ERV3 Double Nickase Plasmid (h) | sc-410773-NIC | 20 µg | $410.00 | |||
ERV3 Double Nickase Plasmid (h2) | sc-410773-NIC-2 | 20 µg | $410.00 |
ERV3-1 encodes ERV3, an envelope-like protein derived from an endogenous retroviral element that is transcriptionally active in select human tissues. As a retroelement-associated gene product, ERV3 has been studied in the context of host–retroelement interactions, regulation of gene expression, and cellular programs linked to differentiation and immune signaling. ERV3 expression has been reported in hematopoietic and placental contexts, motivating investigation into how endogenous retroviral envelopes interface with innate immune pathways and membrane-associated processes. Dysregulated expression of endogenous retroviral genes, including ERV3-1, has been associated in the literature with inflammatory and oncologic settings, supporting its use as a target for mechanistic studies of disease-relevant transcriptional states.
ERV3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ERV3-1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ERV3-1. 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 ERV3-1 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 ERV3-1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.