c-Abl Double Nickase Plasmid (m): sc-418935-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- c-Abl Double Nickase Plasmid (m) 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
- c-Abl Double Nickase Plasmid (m) and c-Abl Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Abl1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
c-Abl Double Nickase Plasmid (m) | sc-418935-NIC | 20 µg | $410.00 | |||
c-Abl Double Nickase Plasmid (m2) | sc-418935-NIC-2 | 20 µg | $410.00 |
Mouse Abl1 encodes the non-receptor tyrosine kinase c-Abl, a multifunctional signaling node that integrates growth factor and integrin cues to regulate cytoskeletal remodeling, cell adhesion and migration, endocytosis, and cell-cycle checkpoint control. c-Abl activity interfaces with DNA damage signaling and stress-response pathways, modulating phosphorylation-dependent networks that influence apoptosis, differentiation, and transcriptional programs. Dysregulated Abl1/c-Abl signaling and altered kinase control are widely studied in oncogenic transformation and aberrant proliferative signaling, while perturbations in c-Abl-dependent actin dynamics are relevant to invasion and tissue remodeling. In mouse models, Abl1 is frequently leveraged to dissect kinase-driven signaling circuitry and to link genotoxic stress responses with changes in cell fate.
c-Abl Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Abl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Abl1. 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 Abl1 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 Abl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.