TBC1D15 Double Nickase Plasmid (m): sc-426147-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TBC1D15 Double Nickase Plasmid (m) 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
- TBC1D15 Double Nickase Plasmid (m) and TBC1D15 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tbc1d15. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TBC1D15 Double Nickase Plasmid (m) | sc-426147-NIC | 20 µg | $410.00 |
Tbc1d15 encodes TBC1D15, a Rab GTPase-activating protein implicated in the control of intracellular membrane trafficking and organelle dynamics. In mouse cells, TBC1D15 has been linked to mitochondrial homeostasis, including regulation of mitochondrial morphology and turnover, and it interfaces with pathways governing autophagy/mitophagy and endolysosomal transport. By modulating Rab-dependent trafficking steps, TBC1D15 can influence cellular stress responses and metabolic adaptation. Dysregulation of these processes is relevant to studies of neurodegeneration, inflammation, and cancer cell biology where altered mitochondrial quality control and vesicle trafficking contribute to pathogenic mechanisms.
TBC1D15 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tbc1d15 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tbc1d15. 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 Tbc1d15 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 Tbc1d15-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.