Date published: 2026-7-4

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PFKL CRISPR/Cas9 KO Plasmid (h): sc-402662

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • PFKL 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 PFKL 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: PFKL Antibody (A-6): sc-393713
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    PFKL CRISPR/Cas9 KO Plasmid (h)

    sc-402662
    20 µg
    $397.00

    Overview

    PFKL encodes the liver isoform of phosphofructokinase-1 (PFK-1), a key rate-limiting enzyme that catalyzes the conversion of fructose-6-phosphate to fructose-1,6-bisphosphate in glycolysis. By integrating allosteric inputs from cellular energy and metabolite status, PFKL helps coordinate glycolytic flux with biosynthetic demands and redox balance. Altered PFKL activity and expression have been linked to metabolic reprogramming in proliferative states, contributing to changes in glucose utilization, lactate production, and downstream carbon routing. As a central node in glycolysis, PFKL is frequently investigated in studies of energy homeostasis, stress adaptation, and metabolic dependencies relevant to disease-associated phenotypes.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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