Date published: 2026-7-14

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p35 CRISPR/Cas9 KO Plasmid (h): sc-400431

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • p35 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 p35 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: p35 Antibody (B-1): sc-518009
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    p35 CRISPR/Cas9 KO Plasmid (h)

    sc-400431
    20 µg
    $397.00

    Overview

    CDK5R1 encodes p35, a neuron-enriched regulatory subunit that binds and activates cyclin-dependent kinase 5 (CDK5) to control spatiotemporal kinase activity at membranes and within neurites. The CDK5–p35 complex coordinates neuronal migration, axon guidance, synaptogenesis, and activity-dependent synaptic plasticity through phosphorylation of cytoskeletal and signaling proteins, linking it to pathways governing microtubule and actin dynamics. Dysregulated p35 turnover and conversion to p25 can prolong CDK5 activity and perturb proteostasis, contributing to mechanisms studied in neurodegeneration and excitotoxic stress. Altered CDK5R1 expression or CDK5–p35 signaling has also been examined in contexts such as epilepsy, neurodevelopmental phenotypes, and neuronal injury responses.

    p35 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CDK5R1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CDK5R1 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 CDK5R1 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 p35 protein expression.

    This CRISPR knockout system enables efficient generation of CDK5R1-deficient cell models for investigation of p35 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting CDK5R1 exon(s) critical for p35 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 CDK5R1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by p35 CRISPR/Cas9 KO Plasmid (h) and p35 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CDK5R1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by p35 HDR Plasmid (h) and p35 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CDK5R1 homology arms to support homology-directed repair at defined CDK5R1 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.