Date published: 2026-8-15

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HSP 78 CRISPR/Cas9 KO Plasmid (h): sc-413434

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • HSP 78 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 HSP 78 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

    HSP 78 CRISPR/Cas9 KO Plasmid (h)

    sc-413434
    20 µg
    $397.00

    Overview

    CLPB encodes the human mitochondrial AAA+ chaperone HSP 78, a protein disaggregase that cooperates with mitochondrial HSP70/HSP60 systems to extract and refold misfolded or aggregated proteins in the matrix. Through ATP-dependent remodeling of protein complexes, CLPB supports mitochondrial proteostasis, respiratory chain integrity, and cellular adaptation to proteotoxic and oxidative stress. CLPB-linked dysfunction has been associated with mitochondrial disease phenotypes and altered metabolic homeostasis, underscoring its relevance to pathways controlling energy production, stress responses, and quality control. As a node in mitochondrial protein surveillance, HSP 78 is frequently studied in contexts involving impaired oxidative phosphorylation, redox imbalance, and stress-induced apoptosis signaling.

    HSP 78 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CLPB gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CLPB 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 CLPB 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 HSP 78 protein expression.

    This CRISPR knockout system enables efficient generation of CLPB-deficient cell models for investigation of HSP 78 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting CLPB exon(s) critical for HSP 78 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 CLPB genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by HSP 78 CRISPR/Cas9 KO Plasmid (h) and HSP 78 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CLPB locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by HSP 78 HDR Plasmid (h) and HSP 78 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CLPB homology arms to support homology-directed repair at defined CLPB 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.