Date published: 2026-7-11

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TERT CRISPR/Cas9 KO Plasmid (m): sc-423341

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TERT 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 TERT 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: TERT Antibody (C-12): sc-377511
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TERT CRISPR/Cas9 KO Plasmid (m)

    sc-423341
    20 µg
    $397.00

    Overview

    Tert encodes the catalytic subunit of telomerase (TERT), a reverse transcriptase that extends telomeric repeats to preserve chromosome ends during DNA replication. By maintaining telomere length, TERT supports long-term proliferative capacity and influences genome stability, replicative senescence, and cellular stress responses. TERT activity intersects with DNA damage signaling and telomere protection pathways, including shelterin-mediated end capping and checkpoint regulation. Dysregulated telomerase function is relevant to aging-associated phenotypes, stem cell biology, and tumorigenesis models where telomere maintenance impacts chromosomal instability and cell fate.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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