SURF-4 Double Nickase Plasmid (h): sc-407135-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SURF-4 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
- SURF-4 Double Nickase Plasmid (h) and SURF-4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SURF4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SURF-4 Double Nickase Plasmid (h) | sc-407135-NIC | 20 µg | $410.00 |
SURF4 encodes SURF-4, an endoplasmic reticulum (ER) membrane protein implicated in early secretory pathway regulation and cargo selection at ER exit sites. SURF-4 participates in ER-to-Golgi transport processes that coordinate proteostasis and influence the abundance and trafficking of select secreted and membrane-associated proteins. Through its role in secretory cargo handling, SURF-4 connects to cellular pathways governing ER homeostasis, protein quality control, and lipid/protein trafficking dynamics. Dysregulation of secretory pathway components such as SURF-4 is relevant to research on metabolic and proteostasis-associated disorders where altered secretion and ER stress responses contribute to disease mechanisms.
SURF-4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SURF4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SURF4. 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 SURF4 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 SURF4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.