Atg2B CRISPR/Cas9 KO Plasmid (m): sc-429358
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Atg2B 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 Atg2B 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 | |
Atg2B CRISPR/Cas9 KO Plasmid (m) | sc-429358 | 20 µg | $397.00 |
Overview
Atg2b encodes the autophagy-related protein Atg2B, a conserved factor required for autophagosome biogenesis and maturation. Atg2B functions in lipid handling at membrane contact sites, supporting phagophore expansion and efficient autophagic flux, processes that integrate nutrient sensing and organelle quality control. Disruption of autophagy pathways involving Atg2B can perturb proteostasis, mitochondrial homeostasis, and innate immune signaling, connecting this gene to mechanisms relevant to neurodegeneration, cancer biology, and inflammatory phenotypes in experimental models. In mouse systems, Atg2b is therefore widely studied for its role in cellular stress adaptation and turnover of damaged macromolecules.
Atg2B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Atg2b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Atg2b 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 Atg2b 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 Atg2B protein expression.
This CRISPR knockout system enables efficient generation of Atg2b-deficient cell models for investigation of Atg2B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Atg2b exon(s) critical for Atg2B 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 Atg2b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Atg2B CRISPR/Cas9 KO Plasmid (m) and Atg2B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Atg2b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Atg2B HDR Plasmid (m) and Atg2B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Atg2b homology arms to support homology-directed repair at defined Atg2b 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.