Date published: 2026-7-8

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RTEL1 CRISPR/Cas9 KO Plasmid (h): sc-403196

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • RTEL1 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 RTEL1 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: RTEL1 Antibody (H-5): sc-515427
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    RTEL1 CRISPR/Cas9 KO Plasmid (h)

    sc-403196
    20 µg
    $397.00

    Overview

    RTEL1 encodes Regulator of Telomere Elongation Helicase 1, a DNA helicase that preserves genome stability by promoting faithful DNA replication and repair. RTEL1 dismantles aberrant DNA secondary structures such as G-quadruplexes and resolves telomeric T-loops, supporting telomere maintenance and preventing inappropriate recombination. It functions in pathways linked to replication fork progression, homologous recombination control, and DNA damage response signaling. Disruption of RTEL1 activity is associated with telomere dysfunction and genomic instability phenotypes implicated in inherited telomere biology disorders and cancer susceptibility.

    RTEL1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RTEL1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RTEL1 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 RTEL1 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 RTEL1 protein expression.

    This CRISPR knockout system enables efficient generation of RTEL1-deficient cell models for investigation of RTEL1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting RTEL1 exon(s) critical for RTEL1 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 RTEL1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by RTEL1 CRISPR/Cas9 KO Plasmid (h) and RTEL1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RTEL1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by RTEL1 HDR Plasmid (h) and RTEL1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RTEL1 homology arms to support homology-directed repair at defined RTEL1 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.