ATAD1 CRISPR/Cas9 KO Plasmid (h): sc-413720
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATAD1 CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the ATAD1 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATAD1 CRISPR/Cas9 KO Plasmid (h) | sc-413720 | 20 µg | $397.00 |
Overview
ATAD1 (ATPase family AAA domain containing 1) is a mitochondrial outer membrane AAA+ ATPase that functions in protein quality control by extracting and clearing mislocalized or damaged tail-anchored proteins from the membrane. Through its ATP-dependent dislocase activity, ATAD1 supports mitochondrial homeostasis, coordinates with ubiquitin–proteasome pathways, and influences organelle stress responses that impact cellular metabolism and survival. Perturbation of ATAD1-dependent membrane protein surveillance can alter mitochondrial dynamics and proteostasis, processes frequently studied in the context of neurodegeneration, metabolic dysregulation, and cancer-associated mitochondrial remodeling. As a regulator of mitochondrial protein turnover, ATAD1 is a useful node for investigating how organelle quality control intersects with apoptosis signaling and cellular stress adaptation.
ATAD1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ATAD1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ATAD1 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the ATAD1 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish ATAD1 protein expression.
This CRISPR knockout system enables efficient generation of ATAD1-deficient cell models for investigation of ATAD1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ATAD1 exon(s) critical for ATAD1 function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple ATAD1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ATAD1 CRISPR/Cas9 KO Plasmid (h) and ATAD1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ATAD1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ATAD1 HDR Plasmid (h) and ATAD1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ATAD1 homology arms to support homology-directed repair at defined ATAD1 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.