Atg9a CRISPR/Cas9 KO Plasmid (m): sc-434176
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Atg9a CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 Atg9a 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 | |
Atg9a CRISPR/Cas9 KO Plasmid (m) | sc-434176 | 20 µg | $397.00 |
Overview
Atg9a encodes ATG9A, a conserved multispanning membrane protein that traffics between the trans-Golgi network, endosomes, and nascent autophagosomes to support membrane delivery during macroautophagy. It functions within core autophagy machinery regulating phagophore expansion and autophagosome biogenesis, integrating cues from nutrient-sensing and stress-responsive pathways that influence lysosomal turnover. In mouse systems, altered Atg9a activity is used to probe autophagy-dependent control of protein and organelle quality, including mitophagy and ER homeostasis. Dysregulated ATG9A-associated autophagy has been linked to neurodegeneration, infection biology, and inflammatory phenotypes, making it relevant for mechanistic studies of cellular stress and tissue maintenance.
Atg9a CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Atg9a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Atg9a 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 Atg9a 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 Atg9a protein expression.
This CRISPR knockout system enables efficient generation of Atg9a-deficient cell models for investigation of Atg9a signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Atg9a exon(s) critical for Atg9a 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 Atg9a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Atg9a CRISPR/Cas9 KO Plasmid (m) and Atg9a CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Atg9a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Atg9a HDR Plasmid (m) and Atg9a HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Atg9a homology arms to support homology-directed repair at defined Atg9a 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.