Src Double Nickase Plasmid (h): sc-400165-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Src 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
- Src Double Nickase Plasmid (h) and Src Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SRC. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Src Antibody (H-12): sc-5266
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Src Double Nickase Plasmid (h) | sc-400165-NIC | 20 µg | $410.00 | |||
Src Double Nickase Plasmid (h2) | sc-400165-NIC-2 | 20 µg | $410.00 |
Human SRC encodes Src, a non-receptor tyrosine kinase that integrates signals from receptor tyrosine kinases, integrins, and immune receptors to regulate proliferation, survival, adhesion, and cytoskeletal remodeling. Src activity propagates through pathways such as RAS–MAPK, PI3K–AKT, and focal adhesion signaling, shaping cell migration and mechanotransduction. Dysregulated SRC signaling is frequently associated with oncogenic phenotypes including enhanced invasion, epithelial–mesenchymal transition programs, and altered interactions with the tumor microenvironment. SRC is also used as a model kinase for studying phosphorylation-dependent signaling networks and feedback control in diverse human cell types.
Src Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SRC locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SRC. 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 SRC 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 SRC-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.