Date published: 2026-9-17

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trichoplein CRISPR/Cas9 KO Plasmid (h): sc-407983

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • trichoplein 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 trichoplein 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: trichoplein Antibody (G-2): sc-515025
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    trichoplein CRISPR/Cas9 KO Plasmid (h)

    sc-407983
    20 µg
    $397.00

    Overview

    TCHP encodes trichoplein, a centriolar and microtubule-associated protein that regulates centrosome function and primary cilium dynamics, linking cell-cycle progression to ciliary signaling. Trichoplein has been implicated in control of ciliogenesis through interactions with cell-cycle kinases and centrosomal regulators, influencing cytoskeletal organization and mitotic fidelity. Through its effects on cilia-dependent pathways and centrosome integrity, altered TCHP activity can perturb proliferation, differentiation, and stress responses. Dysregulation of cilia/centrosome homeostasis is relevant to mechanistic studies of developmental disorders and cancer-associated phenotypes, making TCHP a useful node for pathway interrogation.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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