EGR1 Double Nickase Plasmid (h): sc-400133-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EGR1 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
- EGR1 Double Nickase Plasmid (h) and EGR1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting EGR1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: EGR1 Antibody (S-25): sc-101033
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EGR1 Double Nickase Plasmid (h) | sc-400133-NIC | 20 µg | $410.00 | |||
EGR1 Double Nickase Plasmid (h2) | sc-400133-NIC-2 | 20 µg | $410.00 |
EGR1 (early growth response 1) encodes an immediate-early zinc finger transcription factor rapidly induced by mitogens, cytokines, and cellular stress. It integrates signaling from MAPK/ERK and related pathways to regulate transcriptional programs controlling proliferation, differentiation, apoptosis, and wound-response genes. EGR1 modulates inflammatory and growth-factor networks, including cross-talk with TGF-β and NF-κB-regulated responses, shaping cell fate decisions and tissue remodeling. Dysregulated EGR1 activity has been associated with cancer biology, vascular and fibrotic remodeling, and neurological stress responses, making it a useful node for mechanistic studies of stimulus-dependent transcription.
EGR1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the EGR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within EGR1. 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 EGR1 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 EGR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.