Date published: 2026-8-29

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AFG3L2 CRISPR/Cas9 KO Plasmid (h): sc-404565

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • AFG3L2 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 AFG3L2 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    AFG3L2 CRISPR/Cas9 KO Plasmid (h)

    sc-404565
    20 µg
    $397.00

    Overview

    AFG3L2 encodes a mitochondrial inner membrane AAA+ metalloprotease that assembles into the m-AAA protease complex, supporting protein quality control by extracting and degrading misfolded or unassembled membrane proteins. Through regulated proteolysis, AFG3L2 helps maintain respiratory chain integrity, mitochondrial ribosome biogenesis, and overall oxidative phosphorylation capacity, thereby influencing cellular energy metabolism and proteostasis. Disruption of AFG3L2 function perturbs mitochondrial dynamics and can trigger stress responses linked to impaired bioenergetics. Pathogenic variants in AFG3L2 are associated with neurodegenerative phenotypes, including spinocerebellar ataxia, making it a useful target for studying mitochondrial dysfunction in neuronal models.

    AFG3L2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the AFG3L2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the AFG3L2 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 AFG3L2 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 AFG3L2 protein expression.

    This CRISPR knockout system enables efficient generation of AFG3L2-deficient cell models for investigation of AFG3L2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting AFG3L2 exon(s) critical for AFG3L2 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 AFG3L2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by AFG3L2 CRISPR/Cas9 KO Plasmid (h) and AFG3L2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the AFG3L2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by AFG3L2 HDR Plasmid (h) and AFG3L2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by AFG3L2 homology arms to support homology-directed repair at defined AFG3L2 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.