Date published: 2026-7-9

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CYTIP CRISPR/Cas9 KO Plasmid (h): sc-411299

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CYTIP 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 CYTIP 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: CYTIP Antibody (B-3): sc-514829
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CYTIP CRISPR/Cas9 KO Plasmid (h)

    sc-411299
    20 µg
    $397.00

    Overview

    CYTIP (cytohesin-1 interacting protein) is a cytoplasmic adaptor enriched in immune cells that modulates inside-out signaling to integrins and supports leukocyte adhesion, polarization, and migration. By binding cytohesin-1, CYTIP can influence ARF GTPase–dependent membrane trafficking and actin cytoskeleton remodeling, linking receptor-triggered signaling to changes in cell motility and immune synapse organization. CYTIP is implicated in pathways governing T cell activation and dendritic cell function, where altered expression can shift immune cell recruitment and effector responses. Dysregulation of CYTIP-associated signaling has been studied in the context of inflammatory processes and tumor-immune interactions, making it relevant for mechanistic immunology and cancer microenvironment research.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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