ATAD1 Double Nickase Plasmid (h): sc-413720-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATAD1 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
- ATAD1 Double Nickase Plasmid (h) and ATAD1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATAD1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATAD1 Double Nickase Plasmid (h) | sc-413720-NIC | 20 µg | $410.00 | |||
ATAD1 Double Nickase Plasmid (h2) | sc-413720-NIC-2 | 20 µg | $410.00 |
ATAD1 (ATPase family AAA domain-containing protein 1) is a membrane-anchored AAA+ ATPase that localizes primarily to the mitochondrial outer membrane, where it supports protein quality control by extracting mislocalized or stalled tail-anchored proteins and coordinating their turnover. Through ATP-dependent remodeling and crosstalk with ubiquitin–proteasome pathways, ATAD1 helps maintain mitochondrial proteostasis, organelle integrity, and cellular homeostasis under proteotoxic or metabolic stress. Disruption of ATAD1-dependent surveillance can perturb mitochondrial dynamics and bioenergetic function, linking this factor to broader stress-response networks that influence cell survival and differentiation. Altered ATAD1 activity and copy-number changes have been investigated in the context of tumor biology and neurodegenerative phenotypes where mitochondrial dysfunction is a central feature.
ATAD1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATAD1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATAD1. 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 ATAD1 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 ATAD1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.