REPS1 Double Nickase Plasmid (h): sc-409347-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- REPS1 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
- REPS1 Double Nickase Plasmid (h) and REPS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting REPS1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
REPS1 Double Nickase Plasmid (h) | sc-409347-NIC | 20 µg | $410.00 |
REPS1 (RALBP1-associated Eps domain-containing protein 1) encodes an adaptor protein implicated in clathrin-mediated endocytosis and receptor trafficking through interactions with RalBP1/RLIP76 and endocytic accessory factors. By coupling small GTPase signaling to vesicle formation and cargo internalization, REPS1 can influence downstream pathways that depend on regulated receptor availability, including growth factor and stress-response signaling. REPS1-associated processes intersect with cytoskeletal dynamics and membrane remodeling, linking it to cellular migration, adhesion, and signal attenuation. Dysregulation of endocytic adaptors and Ral pathway components has been associated with altered proliferative signaling and invasive phenotypes in cancer biology, motivating mechanistic studies of REPS1 function in human cell models.
REPS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the REPS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within REPS1. 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 REPS1 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 REPS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.