Date published: 2026-7-14

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HARE CRISPR/Cas9 KO Plasmid (h): sc-405069

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • HARE 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 HARE 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: HARE Antibody (B-2): sc-398732
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    HARE CRISPR/Cas9 KO Plasmid (h)

    sc-405069
    20 µg
    $397.00

    Overview

    STAB2 encodes hyaluronan receptor for endocytosis (HARE), a multifunctional scavenger receptor predominantly expressed on liver sinusoidal endothelial cells and select macrophage-lineage populations. HARE mediates clathrin-dependent uptake and lysosomal clearance of hyaluronan and diverse anionic ligands, linking extracellular matrix turnover to receptor-mediated endocytosis and vascular homeostasis. Through regulation of hyaluronan catabolism and trafficking of circulating glycosaminoglycans, STAB2 influences inflammatory signaling, leukocyte adhesion dynamics, and tissue remodeling programs. Altered STAB2 activity has been associated with dysregulated hyaluronan handling in fibrosis and inflammatory disease contexts, supporting its use as a mechanistic node in matrix biology and clearance pathway studies.

    HARE CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the STAB2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the STAB2 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 STAB2 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 HARE protein expression.

    This CRISPR knockout system enables efficient generation of STAB2-deficient cell models for investigation of HARE signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting STAB2 exon(s) critical for HARE 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 STAB2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by HARE CRISPR/Cas9 KO Plasmid (h) and HARE CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the STAB2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by HARE HDR Plasmid (h) and HARE HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by STAB2 homology arms to support homology-directed repair at defined STAB2 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.