TECPR1 Double Nickase Plasmid (h): sc-409865-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TECPR1 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
- TECPR1 Double Nickase Plasmid (h) and TECPR1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TECPR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TECPR1 Double Nickase Plasmid (h) | sc-409865-NIC | 20 µg | $410.00 | |||
TECPR1 Double Nickase Plasmid (h2) | sc-409865-NIC-2 | 20 µg | $410.00 |
TECPR1 (tectonin beta-propeller repeat containing 1) is a cytosolic adaptor that binds autophagy machinery and contributes to selective autophagy, including the recognition and trafficking of cargo toward lysosomal degradation. Through interactions with core autophagy components, TECPR1 supports autophagosome maturation and membrane dynamics that help maintain proteostasis and cellular stress tolerance. TECPR1-dependent pathways are relevant to innate defense against intracellular microbes and to neuronal homeostasis where disrupted autophagy can promote accumulation of toxic proteins and organelle damage. Altered TECPR1 function has been associated with neurodevelopmental phenotypes and provides a mechanistic entry point for studying how autophagy defects intersect with inflammation and degeneration.
TECPR1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TECPR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TECPR1. 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 TECPR1 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 TECPR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.