Arg Double Nickase Plasmid (h): sc-417779-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Arg 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
- Arg Double Nickase Plasmid (h) and Arg Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ABL2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Arg Antibody (1H1B11): sc-81154
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Arg Double Nickase Plasmid (h) | sc-417779-NIC | 20 µg | $410.00 |
Human ABL2 encodes the non-receptor tyrosine kinase Arg, a cytoplasmic signaling protein that integrates cues from growth factor receptors and adhesion complexes to regulate actin cytoskeleton remodeling, membrane protrusion, and cell motility. Arg phosphorylates multiple cytoskeletal and adaptor proteins, linking kinase signaling to processes such as endocytosis, axon guidance, and focal adhesion turnover. Through its SH3/SH2 and kinase domains, Arg participates in pathways downstream of integrins and receptor tyrosine kinases that influence migration, invasion-related behaviors, and cellular stress responses. Dysregulated ABL-family kinase activity and altered Arg-dependent cytoskeletal control have been associated with oncogenic signaling programs and aberrant cell movement phenotypes in cancer biology research.
Arg Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ABL2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ABL2. 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 ABL2 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 ABL2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.