Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
RSAD2 Double Nickase Plasmid (h): sc-402884-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RSAD2 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
- RSAD2 Double Nickase Plasmid (h) and RSAD2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RSAD2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RSAD2 Antibody (G-8): sc-390342
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RSAD2 Double Nickase Plasmid (h) | sc-402884-NIC | 20 µg | $410.00 |
RSAD2 (also known as viperin) encodes an interferon-inducible radical S-adenosyl‑L‑methionine (SAM) enzyme that localizes primarily to the endoplasmic reticulum and lipid droplet–associated membranes to coordinate innate antiviral responses. RSAD2 is induced downstream of pattern-recognition receptor signaling and type I/III interferon pathways, and it can modulate cellular lipid metabolism and membrane organization that influence pathogen replication. Through interactions with innate immune signaling components and effects on metabolic networks, RSAD2 contributes to regulation of interferon-stimulated gene programs and inflammatory signaling dynamics. Dysregulated RSAD2 expression has been reported across viral infection contexts and immune-associated pathologies, making it a useful node for studying host–pathogen interactions and interferon-driven transcriptional states.
RSAD2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RSAD2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RSAD2. 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 RSAD2 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 RSAD2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.