Date published: 2026-8-26

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LYPLA3 CRISPR/Cas9 KO Plasmid (h): sc-409535

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • LYPLA3 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 LYPLA3 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
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LYPLA3 Antibody (B-2): sc-376078
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    LYPLA3 CRISPR/Cas9 KO Plasmid (h)

    sc-409535
    20 µg
    $397.00

    Overview

    PLA2G15 encodes LYPLA3, a lysosomal phospholipase/deacylase implicated in phospholipid turnover and the remodeling of membrane lipids through hydrolysis of fatty acyl chains. By contributing to lysosomal lipid catabolism, LYPLA3 intersects with pathways that govern endolysosomal trafficking, autophagy-linked degradation, and cellular lipid homeostasis. Dysregulated lysosomal lipid processing is broadly relevant to metabolic stress responses and can influence inflammatory signaling and organelle function, making LYPLA3 a useful node for studying lipid-driven perturbations in human cells. Functional interrogation of LYPLA3 supports mechanistic studies of lipid metabolism and lysosome-centered processes that are frequently altered in disease-associated cellular states.

    LYPLA3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PLA2G15 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PLA2G15 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 PLA2G15 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 LYPLA3 protein expression.

    This CRISPR knockout system enables efficient generation of PLA2G15-deficient cell models for investigation of LYPLA3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting PLA2G15 exon(s) critical for LYPLA3 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 PLA2G15 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by LYPLA3 CRISPR/Cas9 KO Plasmid (h) and LYPLA3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PLA2G15 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by LYPLA3 HDR Plasmid (h) and LYPLA3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PLA2G15 homology arms to support homology-directed repair at defined PLA2G15 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.