Date published: 2026-7-12

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p22HBP CRISPR/Cas9 KO Plasmid (m): sc-420826

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • p22HBP CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 p22HBP 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: p22HBP Antibody (B-3): sc-398612
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    p22HBP CRISPR/Cas9 KO Plasmid (m)

    sc-420826
    20 µg
    $397.00

    Overview

    Mouse Hebp1 encodes p22HBP, a heme-binding protein implicated in intracellular heme trafficking and heme-dependent redox regulation. p22HBP has been linked to mitochondrial-associated processes, oxidative stress responses, and modulation of apoptosis, consistent with roles in maintaining cellular homeostasis under metabolic stress. Through interactions with heme and heme-derived signaling, Hebp1 may influence pathways tied to reactive oxygen species balance, mitochondrial function, and protein quality control. Dysregulation of heme handling and oxidative injury are relevant to neurodegeneration and inflammatory tissue damage, making Hebp1 a useful target for mechanistic studies in these contexts.

    p22HBP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Hebp1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Hebp1 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 Hebp1 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 p22HBP protein expression.

    This CRISPR knockout system enables efficient generation of Hebp1-deficient cell models for investigation of p22HBP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Hebp1 exon(s) critical for p22HBP 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 Hebp1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by p22HBP CRISPR/Cas9 KO Plasmid (m) and p22HBP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Hebp1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by p22HBP HDR Plasmid (m) and p22HBP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Hebp1 homology arms to support homology-directed repair at defined Hebp1 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.