Date published: 2026-7-15

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CLK4 CRISPR/Cas9 KO Plasmid (m): sc-419690

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CLK4 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 CLK4 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CLK4 CRISPR/Cas9 KO Plasmid (m)

    sc-419690
    20 µg
    $397.00

    Overview

    Clk4 encodes CDC-like kinase 4 (CLK4), a dual-specificity kinase that phosphorylates serine/arginine-rich (SR) splicing factors and helps coordinate pre-mRNA splicing with transcriptional programs. By modulating SR protein activity, CLK4 contributes to alternative splicing choices that influence cell cycle progression, differentiation, and stress-responsive gene expression. CLK family signaling intersects with RNA processing networks that shape proteome diversity, and altered splicing regulation is commonly linked to oncogenic transformation and neurodevelopmental phenotypes in experimental models. In mouse systems, perturbing Clk4 provides a tractable route to dissect how spliceosome-associated phosphorylation dynamics affect tissue-specific transcript isoforms and downstream pathway outputs.

    CLK4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Clk4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Clk4 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 Clk4 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 CLK4 protein expression.

    This CRISPR knockout system enables efficient generation of Clk4-deficient cell models for investigation of CLK4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Clk4 exon(s) critical for CLK4 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 Clk4 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by CLK4 CRISPR/Cas9 KO Plasmid (m) and CLK4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Clk4 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by CLK4 HDR Plasmid (m) and CLK4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Clk4 homology arms to support homology-directed repair at defined Clk4 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.