Fra1 Double Nickase Plasmid (h): sc-400527-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Fra1 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
- Fra1 Double Nickase Plasmid (h) and Fra1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FOSL1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Fra1 Antibody (D-3): sc-376148
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Fra1 Double Nickase Plasmid (h) | sc-400527-NIC | 20 µg | $410.00 | |||
Fra1 Double Nickase Plasmid (h2) | sc-400527-NIC-2 | 20 µg | $410.00 |
Human FOSL1 encodes Fra1 (FOS-like antigen 1), a JUN dimerization partner that forms AP-1 transcription factor complexes controlling stimulus-responsive gene expression. Fra1 integrates signals from MAPK/ERK and related kinase cascades to regulate programs involved in cell-cycle progression, differentiation, extracellular matrix remodeling, and inflammatory responses. Altered FOSL1 activity is frequently linked to oncogenic transcriptional states, epithelial–mesenchymal transition, and invasive phenotypes, and it is also implicated in fibrotic and immune-driven pathologies. Consequently, Fra1 is widely studied as a pathway-responsive node connecting mitogenic signaling to transcriptional reprogramming.
Fra1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FOSL1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FOSL1. 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 FOSL1 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 FOSL1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.