Date published: 2026-7-2

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hnRNP R CRISPR/Cas9 KO Plasmid (h): sc-404489

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • hnRNP R 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 hnRNP R 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

    hnRNP R CRISPR/Cas9 KO Plasmid (h)

    sc-404489
    20 µg
    $397.00

    Overview

    HNRNPR encodes the human heterogeneous nuclear ribonucleoprotein R (hnRNP R), an RNA-binding protein that associates with nascent transcripts and ribonucleoprotein complexes to regulate pre-mRNA processing, mRNA stability, and subcellular RNA localization. hnRNP R contributes to post-transcriptional gene regulation through interactions that influence alternative splicing and RNA transport, linking nuclear RNA metabolism to cytoplasmic translation control. Dysregulation of RNA-binding proteins and splicing-associated networks is implicated in neurodegenerative and neuromuscular disease mechanisms, making HNRNPR a useful node for studying RNA homeostasis. Experimental interrogation of hnRNP R supports pathway-level analyses of transcriptome remodeling, stress-responsive RNA granule dynamics, and proteostasis-related phenotypes.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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