eIF4AI Double Nickase Plasmid (h): sc-402623-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- eIF4AI 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
- eIF4AI Double Nickase Plasmid (h) and eIF4AI Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting EIF4A1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
eIF4AI Double Nickase Plasmid (h) | sc-402623-NIC | 20 µg | $410.00 | |||
eIF4AI Double Nickase Plasmid (h2) | sc-402623-NIC-2 | 20 µg | $410.00 |
EIF4A1 encodes the human eIF4AI DEAD-box RNA helicase, a core component of the eIF4F translation initiation complex that unwinds structured 5′ UTRs to enable 43S preinitiation complex scanning and start-codon recognition. By controlling cap-dependent mRNA translation, eIF4AI influences proteostasis, cell-cycle progression, and stress-adaptive programs, integrating with signaling nodes that modulate initiation such as mTOR/4E-BP and MAPK pathways. Altered EIF4A1 activity and dependency on eIF4A-driven translation are frequently studied in contexts of dysregulated growth and survival, including oncogenic transcriptional programs and stress responses. EIF4A1 is also leveraged as a mechanistic entry point to investigate translational reprogramming, RNA helicase function, and selective translation of complex mRNA subsets.
eIF4AI Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the EIF4A1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within EIF4A1. 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 EIF4A1 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 EIF4A1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.