ArticleMolecular biology of the cell2016
Hsp90 induces increased genomic instability toward DNA-damaging agents by tuning down RAD53 transcription.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Mechanisms of formic acid stress response in evolved yeast for microbial-electrocatalytic systems.Biodesign research · 2026Article
- Inhibition ofFrontiers in parasitology · 2026Article
- Magnetic Hyperthermia Therapy for High-Grade Glioma: A State-of-the-Art Review.Pharmaceuticals (Basel, Switzerland) · 2024Review
- PU-H71 (NSC 750424): a molecular masterpiece that targets HSP90 in cancer and beyond.Frontiers in pharmacology · 2024Review
- Neurosurgical Applications of Magnetic Hyperthermia Therapy.Neurosurgery clinics of North America · 2023Review
- Synergistic Action between PfHsp90 Inhibitor and PfRad51 Inhibitor Induces Elevated DNA Damage Sensitivity in the Malaria Parasite.Antimicrobial agents and chemotherapy · 2021Article
- Lamin-A interacting protein Hsp90 is required for DNA damage repair and chemoresistance of ovarian cancer cells.Cell death & disease · 2021Article
- Pseudohyphal Growth of the Emerging Pathogen Candida auris Is Triggered by Genotoxic Stress through the S Phase Checkpoint.mSphere · 2020Article
- The Nuclear and DNA-Associated Molecular Chaperone Network.Cold Spring Harbor perspectives in biology · 2019Review
- It's not magic - Hsp90 and its effects on genetic and epigenetic variation.Seminars in cell & developmental biology · 2019Review
- Glu-108 in Saccharomyces cerevisiae Rad51 Is Critical for DNA Damage-Induced Nuclear Function.mSphere · 2019Article
- Review
- Hsp90 Is Essential for Chl1-Mediated Chromosome Segregation and Sister Chromatid Cohesion.mSphere · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well documented that elevated body temperature causes tumors to regress upon radiotherapy. However, how hyperthermia induces DNA damage sensitivity is not clear. We show that a transient heat shock and particularly the concomitant induction of Hsp90 lead to increased genomic instability under DNA-damaging conditions. Using Saccharomyces cerevisiae as a model eukaryote, we demonstrate that elevated levels of Hsp90 attenuate efficient DNA damage signaling and dictate preferential use of the potentially mutagenic double-strand break repair pathway. We show that under normal physiological conditions, Hsp90 negatively regulates RAD53 transcription to suppress DNA damage checkpoint activation. However, under DNA damaging conditions, RAD53 is derepressed, and the increased level of Rad53p triggers an efficient DNA damage response. A higher abundance of Hsp90 causes increased transcriptional repression on RAD53 in a dose-dependent manner, which could not be fully derepressed even in the presence of DNA damage. Accordingly, cells behave like a rad53 loss-of-function mutant and show reduced NHEJ efficiency, with a drastic failure to up-regulate RAD51 expression and manifestly faster accumulation of CLN1 and CLN2 in DNA-damaged G1, cells leading to premature release from checkpoint arrest. We further demonstrate that Rad53 overexpression is able to rescue all of the aforementioned deleterious effects caused by Hsp90 overproduction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.