HGK Double Nickase Plasmid (h): sc-403395-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HGK 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
- HGK Double Nickase Plasmid (h) and HGK Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MAP4K4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HGK Antibody (5-12): sc-100445
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HGK Double Nickase Plasmid (h) | sc-403395-NIC | 20 µg | $410.00 |
MAP4K4 encodes the serine/threonine kinase HGK, an upstream regulator of stress-responsive signaling that links membrane-proximal cues to MAPK cascades, including JNK and p38 pathways. HGK contributes to cytoskeletal remodeling, cell migration, inflammatory signaling, and metabolic regulation through modulation of kinase networks and adaptor-dependent signaling nodes. In human cells, altered MAP4K4 activity has been associated with changes in insulin signaling, endothelial and immune cell behavior, and context-dependent effects on proliferation and invasion. These properties make MAP4K4/HGK a useful target for dissecting kinase-driven pathway connectivity and for mapping signaling dependencies in disease-relevant cellular models.
HGK Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MAP4K4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MAP4K4. 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 MAP4K4 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 MAP4K4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.