ERF Double Nickase Plasmid (h): sc-403877-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ERF 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
- ERF Double Nickase Plasmid (h) and ERF Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ERF. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ERF Antibody (E-9): sc-398269
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ERF Double Nickase Plasmid (h) | sc-403877-NIC | 20 µg | $410.00 | |||
ERF Double Nickase Plasmid (h2) | sc-403877-NIC-2 | 20 µg | $410.00 |
ERF (ETS2 repressor factor) is a ubiquitously expressed ETS-family transcription factor that binds GGAA/T motifs to regulate gene programs controlling proliferation, differentiation, and cellular homeostasis. It functions downstream of MAPK/ERK signaling, where phosphorylation-dependent changes in ERF localization and activity modulate transcriptional repression and activation dynamics. ERF contributes to regulation of developmental and hematopoietic pathways and intersects with broader transcriptional networks that influence cell-cycle control and stress responses. Dysregulated ERF activity or expression has been associated with altered MAPK pathway output and implicated in contexts such as craniofacial development phenotypes and cancer-related transcriptional remodeling.
ERF Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ERF locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ERF. 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 ERF 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 ERF-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.