C15orf42 Double Nickase Plasmid (h): sc-409351-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Treslin 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
- Treslin Double Nickase Plasmid (h) and Treslin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TICRR. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C15orf42 Double Nickase Plasmid (h) | sc-409351-NIC | 20 µg | $410.00 | |||
Treslin Double Nickase Plasmid (h2) | sc-409351-NIC-2 | 20 µg | $410.00 |
TICRR, also known as C15orf42, encodes a replication initiation factor that couples S-phase kinase signaling to DNA replication origin firing. The protein supports assembly and activation of the replication machinery through interactions with key replication factors, helping coordinate timely DNA synthesis with checkpoint control. As a component of genome maintenance networks, TICRR function intersects with ATR/CHK1-mediated responses to replication stress and contributes to preserving chromosome stability. Dysregulation of replication initiation and checkpoint signaling linked to TICRR perturbation is relevant to studies of proliferative states, DNA damage responses, and genome instability-associated disease biology.
Treslin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TICRR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TICRR. 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 TICRR 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 TICRR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.