RUFY4 Double Nickase Plasmid (h): sc-405000-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RUFY4 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
- RUFY4 Double Nickase Plasmid (h) and RUFY4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RUFY4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RUFY4 Double Nickase Plasmid (h) | sc-405000-NIC | 20 µg | $410.00 | |||
RUFY4 Double Nickase Plasmid (h2) | sc-405000-NIC-2 | 20 µg | $410.00 |
RUFY4 (RUN and FYVE domain containing 4) encodes a Rab GTPase–interacting effector protein implicated in endosomal membrane trafficking and vesicle maturation. Through its RUN domain and phosphoinositide-binding FYVE-related region, RUFY4 is linked to coordination of vesicular transport, cytoskeletal dynamics, and spatial organization of signaling complexes in immune and epithelial contexts. Expression and functional studies associate RUFY4 with regulation of autophagy-adjacent trafficking steps and inflammatory signaling outputs that shape innate immune responses. Dysregulated endolysosomal transport and immune pathway coupling involving RUFY4 are relevant to mechanistic research in immune dysfunction, neuroinflammation, and cancer cell stress adaptation.
RUFY4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RUFY4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RUFY4. 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 RUFY4 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 RUFY4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.