ATRX Double Nickase Plasmid (m): sc-423734-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATRX 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
- ATRX Double Nickase Plasmid (m) and ATRX Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Atrx. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ATRX Antibody (D-5): sc-55584
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATRX Double Nickase Plasmid (m) | sc-423734-NIC | 20 µg | $410.00 | |||
ATRX Double Nickase Plasmid (m2) | sc-423734-NIC-2 | 20 µg | $410.00 |
Mouse Atrx encodes ATRX, a SWI/SNF-like ATP-dependent chromatin remodeler that partners with DAXX to deposit histone variant H3.3 at repetitive heterochromatin, telomeres, and pericentromeric regions. ATRX helps maintain genome stability by regulating DNA replication dynamics, transcriptional silencing, and DNA damage responses, and it influences higher-order chromatin organization. Disruption of ATRX function is associated with altered epigenetic landscapes and defects in telomere maintenance pathways, making Atrx a widely used model gene for studying chromatin-based mechanisms relevant to neurodevelopmental and cancer-associated phenotypes.
ATRX Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Atrx locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Atrx. 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 Atrx 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 Atrx-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.