Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
TBK1 Double Nickase Plasmid (h): sc-401066-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TBK1 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
- TBK1 Double Nickase Plasmid (h) and TBK1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TBK1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TBK1 Antibody (A-6): sc-398366
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TBK1 Double Nickase Plasmid (h) | sc-401066-NIC | 20 µg | $410.00 | |||
TBK1 Double Nickase Plasmid (h2) | sc-401066-NIC-2 | 20 µg | $410.00 |
TBK1 (TANK-binding kinase 1) is a serine/threonine kinase that integrates innate immune and stress signaling by phosphorylating key substrates such as IRF3/IRF7 to drive type I interferon responses downstream of pattern recognition receptors. It also interfaces with NF-κB signaling via adaptor complexes including TANK, NAP1, and SINTBAD, shaping inflammatory transcriptional programs. Beyond immunity, TBK1 regulates selective autophagy and mitophagy through phosphorylation of autophagy receptors such as optineurin and p62/SQSTM1, linking pathogen sensing to organelle quality control. Genetic and functional perturbation of TBK1 has been associated with neurodegeneration and dysregulated inflammatory states, making it a widely used node for mechanistic studies of immune-autophagy crosstalk.
TBK1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TBK1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TBK1. 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 TBK1 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 TBK1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.