TRIP12 Double Nickase Plasmid (h): sc-403860-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIP12 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
- TRIP12 Double Nickase Plasmid (h) and TRIP12 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRIP12. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRIP12 Double Nickase Plasmid (h) | sc-403860-NIC | 20 µg | $410.00 | |||
TRIP12 Double Nickase Plasmid (h2) | sc-403860-NIC-2 | 20 µg | $410.00 |
TRIP12 encodes an E3 ubiquitin-protein ligase (also known as ULF) that promotes substrate ubiquitination and proteasomal turnover, thereby shaping protein homeostasis and signaling amplitude. It is implicated in DNA damage responses and cell-cycle control through regulation of key checkpoint and tumor suppressor pathways, including modulation of p14ARF–MDM2–p53 axis activity. By influencing ubiquitin-dependent quality control, TRIP12 contributes to genome stability and cellular stress adaptation. Altered TRIP12 function or expression has been associated with dysregulated proliferation and neurodevelopmental phenotypes, making it a relevant target for mechanistic studies in cancer biology and neuronal models.
TRIP12 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRIP12 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRIP12. 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 TRIP12 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 TRIP12-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.