Date published: 2026-7-10

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MFSD2 CRISPR/Cas9 KO Plasmid (m): sc-429366

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • MFSD2 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 MFSD2 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

    MFSD2 CRISPR/Cas9 KO Plasmid (m)

    sc-429366
    20 µg
    $397.00

    Overview

    Mfsd2a encodes MFSD2, a major facilitator superfamily transporter implicated in lipid handling and membrane homeostasis, with well-established roles in endothelial biology and neural tissue physiology. In the blood–brain barrier, MFSD2 contributes to regulation of transcytosis and influences delivery of lysophospholipids such as LPC-linked omega-3 fatty acids, thereby impacting neurovascular unit integrity and neuronal function. Altered MFSD2A activity has been associated with disrupted barrier properties, neurodevelopmental phenotypes, and changes in inflammatory signaling linked to endothelial and metabolic stress. In mouse models, Mfsd2a provides a tractable entry point to study lipid transport–coupled signaling, vascular permeability control, and tissue-specific metabolic adaptation.

    MFSD2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Mfsd2a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Mfsd2a 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 Mfsd2a 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 MFSD2 protein expression.

    This CRISPR knockout system enables efficient generation of Mfsd2a-deficient cell models for investigation of MFSD2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Mfsd2a exon(s) critical for MFSD2 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 Mfsd2a genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by MFSD2 CRISPR/Cas9 KO Plasmid (m) and MFSD2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Mfsd2a locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by MFSD2 HDR Plasmid (m) and MFSD2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Mfsd2a homology arms to support homology-directed repair at defined Mfsd2a 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.