SR-1F Double Nickase Plasmid (h): sc-405459-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SR-1F 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
- SR-1F Double Nickase Plasmid (h) and SR-1F Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HTR1F. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SR-1F Double Nickase Plasmid (h) | sc-405459-NIC | 20 µg | $410.00 | |||
SR-1F Double Nickase Plasmid (h2) | sc-405459-NIC-2 | 20 µg | $410.00 |
HTR1F encodes the human 5-hydroxytryptamine (serotonin) receptor 1F, a G protein-coupled receptor that primarily couples to Gi/Go to inhibit adenylyl cyclase and reduce intracellular cAMP. SR-1F signaling modulates neurotransmitter release and neuronal excitability through cAMP/PKA-regulated processes and downstream effects on ion channel activity and MAPK-associated pathways. Expression of HTR1F is enriched in neuronal tissues and contributes to serotonergic network regulation that influences sensory processing and neurovascular signaling. Dysregulated serotonergic GPCR signaling, including altered HTR1F pathway activity, is implicated in neurologic and neuropsychiatric disease-relevant mechanisms such as migraine biology and sensory circuit dysfunction.
SR-1F Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HTR1F locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HTR1F. 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 HTR1F 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 HTR1F-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.