Atm Double Nickase Plasmid (m): sc-419229-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Atm 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
- Atm Double Nickase Plasmid (m) and Atm Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Atm. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: p-Atm Antibody (10H11.E12): sc-47739
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Atm Double Nickase Plasmid (m) | sc-419229-NIC | 20 µg | $410.00 | |||
Atm Double Nickase Plasmid (m2) | sc-419229-NIC-2 | 20 µg | $410.00 |
Atm encodes a serine/threonine protein kinase that acts as a central sensor and transducer of DNA double-strand break signaling. Upon genotoxic stress, ATM is activated and phosphorylates key substrates including H2AX, CHEK2, TP53, and BRCA1 to coordinate cell-cycle checkpoints, DNA repair pathway choice, chromatin remodeling, and apoptosis. In mouse systems, Atm is widely used to interrogate genome stability networks that influence development, immune diversification, and neuronal integrity. Disruption or hypomorphic function of ATM perturbs the DNA damage response and is strongly linked to cancer susceptibility and neurodegenerative phenotypes in disease models.
Atm Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Atm locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Atm. 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 Atm 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 Atm-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.