Date published: 2026-8-29

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LPAAT-α CRISPR/Cas9 KO Plasmid (h): sc-406544

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

    LPAAT-α CRISPR/Cas9 KO Plasmid (h)

    sc-406544
    20 µg
    $397.00

    Overview

    AGPAT1 encodes lysophosphatidic acid acyltransferase alpha (LPAAT-α), an endoplasmic reticulum–associated acyltransferase that converts lysophosphatidic acid to phosphatidic acid, a central intermediate in glycerophospholipid and triacylglycerol biosynthesis. By regulating phosphatidic acid pools, LPAAT-α influences membrane biogenesis, lipid droplet formation, and downstream lipid signaling that impacts organelle dynamics and cellular stress responses. Perturbation of AGPAT1 activity can alter phospholipid composition and metabolic flux, linking this enzyme to pathways relevant to lipid homeostasis and energy balance. Dysregulated glycerolipid metabolism involving AGPAT1 has been investigated in the context of metabolic and neurodevelopmental phenotypes, making it a useful target for mechanistic studies of lipid-driven cellular processes.

    LPAAT-α CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the AGPAT1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the AGPAT1 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 AGPAT1 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 LPAAT-α protein expression.

    This CRISPR knockout system enables efficient generation of AGPAT1-deficient cell models for investigation of LPAAT-α signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting AGPAT1 exon(s) critical for LPAAT-α 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 AGPAT1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by LPAAT-α CRISPR/Cas9 KO Plasmid (h) and LPAAT-α CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the AGPAT1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by LPAAT-α HDR Plasmid (h) and LPAAT-α HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by AGPAT1 homology arms to support homology-directed repair at defined AGPAT1 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.