Date published: 2026-8-26

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EPI64 CRISPR/Cas9 KO Plasmid (h): sc-407095

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • EPI64 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 EPI64 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: EPI64 Antibody (B-9): sc-376991
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    EPI64 CRISPR/Cas9 KO Plasmid (h)

    sc-407095
    20 µg
    $397.00

    Overview

    TBC1D10A encodes EPI64, a Rab GTPase-activating protein that modulates vesicular trafficking by accelerating GTP hydrolysis on specific Rab family members. Through regulation of endocytic recycling and membrane transport, EPI64 influences receptor turnover, compartment identity, and signal propagation from the plasma membrane to endosomal networks. These processes intersect with cytoskeletal organization and cell migration programs that are frequently rewired in immune signaling and cancer-associated phenotypes. Dysregulated Rab-mediated trafficking has been linked to altered proliferation, invasion, and inflammatory responses, making TBC1D10A a useful node for mechanistic studies of membrane dynamics in human cells.

    EPI64 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TBC1D10A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TBC1D10A 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 TBC1D10A 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 EPI64 protein expression.

    This CRISPR knockout system enables efficient generation of TBC1D10A-deficient cell models for investigation of EPI64 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting TBC1D10A exon(s) critical for EPI64 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 TBC1D10A genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by EPI64 CRISPR/Cas9 KO Plasmid (h) and EPI64 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TBC1D10A locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by EPI64 HDR Plasmid (h) and EPI64 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TBC1D10A homology arms to support homology-directed repair at defined TBC1D10A 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.