ATAD5 Double Nickase Plasmid (h): sc-405654-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATAD5 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
- ATAD5 Double Nickase Plasmid (h) and ATAD5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATAD5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATAD5 Double Nickase Plasmid (h) | sc-405654-NIC | 20 µg | $410.00 | |||
ATAD5 Double Nickase Plasmid (h2) | sc-405654-NIC-2 | 20 µg | $410.00 |
ATAD5 (ATPase family AAA domain-containing protein 5) is a key regulator of genome stability that functions in post-replication repair by facilitating PCNA unloading from chromatin, coordinating replication fork progression and recovery after DNA damage. It acts at the interface of DNA replication and DNA damage tolerance pathways, including template switching and translesion synthesis, thereby limiting replication-associated mutagenesis. Through its role in maintaining replication fidelity and preventing chromosomal instability, ATAD5 is linked to mechanisms relevant to tumorigenesis and other conditions driven by defective DNA repair and replication stress.
ATAD5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATAD5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATAD5. 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 ATAD5 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 ATAD5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.