Tak1 Double Nickase Plasmid (h): sc-400364-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tak1 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
- Tak1 Double Nickase Plasmid (h) and Tak1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MAP3K7. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Tak1 Antibody (C-9): sc-7967
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tak1 Double Nickase Plasmid (h) | sc-400364-NIC | 20 µg | $410.00 | |||
Tak1 Double Nickase Plasmid (h2) | sc-400364-NIC-2 | 20 µg | $410.00 |
MAP3K7 encodes TAK1 (TGF-β–activated kinase 1), a MAP3K that integrates signals from pro-inflammatory cytokines and pattern-recognition receptors to coordinate stress and immune responses. TAK1 phosphorylates downstream MAPK and IKK complexes to regulate NF-κB, JNK, and p38 signaling, shaping transcriptional programs that control inflammation, apoptosis, and cell fate decisions. In human cells, MAP3K7 activity influences innate immune signaling, tissue homeostasis, and responses to genotoxic or oxidative stress, making it relevant to studies of inflammatory dysregulation and oncogenic signaling networks. Genetic perturbation of TAK1 is commonly used to dissect pathway cross-talk between TLR/IL-1R/TNF receptor signaling and MAPK-driven transcriptional regulation.
Tak1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MAP3K7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MAP3K7. 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 MAP3K7 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 MAP3K7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.