TRIP13 Double Nickase Plasmid (h): sc-404006-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIP13 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
- TRIP13 Double Nickase Plasmid (h) and TRIP13 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRIP13. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TRIP13 Antibody (A-7): sc-514285
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRIP13 Double Nickase Plasmid (h) | sc-404006-NIC | 20 µg | $410.00 | |||
TRIP13 Double Nickase Plasmid (h2) | sc-404006-NIC-2 | 20 µg | $410.00 |
TRIP13 (thyroid hormone receptor interactor 13) encodes an AAA+ ATPase that remodels HORMA-domain proteins to regulate spindle assembly checkpoint silencing and ensure accurate chromosome segregation during mitosis. By controlling kinetochore–microtubule attachment stability and checkpoint signaling, TRIP13 supports genome integrity and proper cell-cycle progression. Dysregulated TRIP13 activity has been associated with chromosomal instability and altered proliferative capacity, making it a relevant factor in studies of aneuploidy, DNA damage responses, and tumor biology. Functional interrogation of TRIP13 is therefore informative for pathways linking mitotic surveillance to genomic stability and cell fate decisions.
TRIP13 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRIP13 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRIP13. 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 TRIP13 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 TRIP13-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.