Date published: 2026-9-28

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HiNF-P CRISPR/Cas9 KO Plasmid (h): sc-416760

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • HiNF-P 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 HiNF-P 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: HiNF-P Antibody (C-5): sc-373855
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    HiNF-P CRISPR/Cas9 KO Plasmid (h)

    sc-416760
    20 µg
    $397.00

    Overview

    HINFP encodes the transcription factor HiNF-P, a cell cycle–regulated regulator of histone H4 gene expression that helps coordinate chromatin assembly with DNA replication. HiNF-P functions at S-phase gene promoters and interfaces with transcriptional and epigenetic control programs that maintain genome stability during proliferation. Disruption of HINFP-dependent histone supply can perturb nucleosome deposition, replication timing, and DNA damage responses, linking this pathway to dysregulated growth phenotypes studied in cancer biology and other proliferation-associated disorders. As a human nuclear factor, HiNF-P is commonly investigated in models of cell cycle control, replication stress, and chromatin organization.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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