Date published: 2026-7-4

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HSP90B1/HSP90 beta Double Nickase Plasmid (h): sc-400214-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • HSP90B1/HSP90 beta Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
  • Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
  • One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
  • HSP90B1/HSP90 beta Double Nickase Plasmid (h) and HSP90B1/HSP90 beta Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HSP90AB1. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HSP90B1/HSP90 beta Antibody (AT94B9): sc-517405
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    HSP90B1/HSP90 beta Double Nickase Plasmid (h)

    sc-400214-NIC
    20 µg
    $410.00

    HSP90B1/HSP90 beta Double Nickase Plasmid (h2)

    sc-400214-NIC-2
    20 µg
    $410.00

    HSP90AB1 encodes the cytosolic HSP90 beta (HSP90B1/HSP90 beta), an ATP-dependent molecular chaperone that stabilizes and matures a broad range of client proteins involved in signal transduction, cell-cycle control, and stress responses. As a core component of the proteostasis network, HSP90 beta cooperates with co-chaperones and the ubiquitin–proteasome system to regulate protein folding, quality control, and degradation, influencing pathways such as MAPK/ERK, PI3K–AKT, and DNA damage responses. Perturbation of HSP90 beta function can remodel proteome stability and proteotoxic stress handling, with relevance to studies of oncogenic signaling dependencies, neurodegeneration-associated protein misfolding, and inflammatory or metabolic stress phenotypes. Because many kinases and transcriptional regulators rely on HSP90 activity, HSP90AB1 is frequently used to interrogate chaperone-buffered signaling robustness and cellular adaptation under stress.

    HSP90B1/HSP90 beta Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HSP90AB1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HSP90AB1. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt HSP90AB1 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.

    To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of HSP90AB1-disrupted clones.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.