CHTOP Double Nickase Plasmid (h): sc-411874-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CHTOP 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
- CHTOP Double Nickase Plasmid (h) and CHTOP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CHTOP. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CHTOP Double Nickase Plasmid (h) | sc-411874-NIC | 20 µg | $410.00 | |||
CHTOP Double Nickase Plasmid (h2) | sc-411874-NIC-2 | 20 µg | $410.00 |
CHTOP (chromatin target of PRMT1) is a conserved nuclear protein that couples transcriptional output to RNA processing by participating in messenger ribonucleoprotein assembly and mRNA export. It interacts with the TREX complex and other RNA-binding factors to support co-transcriptional splicing, poly(A)+ RNA maturation, and nucleocytoplasmic transport, linking chromatin-associated events to gene expression programs. Through its regulation of RNA metabolism and epigenetic-associated networks, CHTOP has been studied in contexts where altered transcription and export contribute to cellular stress responses and aberrant proliferation. Dysregulation of CHTOP-associated pathways has been reported across disease-relevant models, making it a useful target for mechanistic studies of RNA processing and genome regulation.
CHTOP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CHTOP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CHTOP. 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 CHTOP 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 CHTOP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.