Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
HSP90B1/HSP90 beta Double Nickase Plasmid (m): sc-420980-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HSP90B1/HSP90 beta Double Nickase Plasmid (m) 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 (m) and HSP90B1/HSP90 beta Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Hsp90ab1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HSP90B1/HSP90 beta Double Nickase Plasmid (m) | sc-420980-NIC | 20 µg | $410.00 | |||
HSP90B1/HSP90 beta Double Nickase Plasmid (m2) | sc-420980-NIC-2 | 20 µg | $410.00 |
Hsp90ab1 encodes the cytosolic HSP90 beta molecular chaperone that supports proteostasis by promoting folding, stabilization, and conformational maturation of a broad client repertoire, including protein kinases, steroid hormone receptors, and signaling adaptors. Through ATP-dependent chaperone cycles with co-chaperones, it contributes to stress responses, protein quality control, and assembly of multiprotein complexes, interfacing with pathways such as MAPK/ERK, PI3K–AKT, and innate immune signaling. Mouse HSP90 beta activity is also linked to cellular homeostasis processes including autophagy and proteasomal turnover, which shape responses to heat shock and oxidative stress. Dysregulated chaperone capacity is frequently studied in the context of oncogenic signaling dependency, neurodegenerative protein misfolding, and inflammatory disease mechanisms, making Hsp90ab1 a useful node for pathway dissection.
HSP90B1/HSP90 beta Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Hsp90ab1 locus in mouse 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.