ReviewOncogene2020
Heat-shock proteins: chaperoning DNA repair.
Review in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
99 citing papers in PubMed, 216 citations in OpenAlex.
- Harnessing genomics approaches for heat stress resilience in wheat: from discovery to deployment.Journal of experimental botany · 2026Review
- Article
- At the Edge of Survival: Exploring the Frontiers of Tardigrade Extreme Stress Tolerance.Molecular ecology · 2026Review
- Hsp70 is phosphorylated in a conserved response to DNA damage and contributes to cell cycle control.eLife · 2026Article
- Heat Shock Proteins as Targets for Cancer Therapeutics.Journal of clinical medicine · 2026Review
- Postnatal temperature triggers predictable thermoregulatory shifts in birds without a trade-off between heat and cold tolerance.The Journal of experimental biology · 2026Article
- Proteostasis, Assisted Reproductive Technologies, and Neurodevelopmental Differences: An Integrative Perspective.Proteomes · 2026Review
- Targeting the Golgi apparatus enhances PD-L1 blockade and synergizes with oxaliplatin to improve immunotherapy efficacy.The Journal of biological chemistry · 2026Article
- Physiological Responses and Heat Tolerance Evaluation of Eight Varieties ofPlants (Basel, Switzerland) · 2026Article
- Self-polymerized polyphenol-based platform for the management of dry eye pathogenesis.Nature communications · 2026Article
- High ambient temperature during pregnancy and offspring cerebral palsy: A population-based case-control study in California.Environmental research · 2026Article
- Amphiphilic Aminated [60] Fullerene Potentiates Radiofrequency Ablation for Synergistic Cancer Treatment.International journal of nanomedicine · 2026Article
- Heat shock proteins in farmed aquatic animals: advancing animal health and welfare management through building resilience.Frontiers in immunology · 2026Review
- Article
- Beyond the ends: potential implications of telomeric repeat-containing RNA (TERRA) for CNS diseases.Journal of molecular cell biology · 2025Review
- A conserved Hsp70 phosphorylation regulates cell cycle progression after DNA damage.bioRxiv : the preprint server for biology · 2025Article
- Stress-inducible phosphoprotein 1 (STIP1) is a critical stemness regulator in mouse embryonic stem cells and early mammalian development.Communications biology · 2025Article
- Article
- Hybrid thiazolyl-benzylidene-phenol metal complexes as novel chemotherapeutic agents with anti-topoisomerase I activity in human breast carcinoma: synthesis,RSC advances · 2025Article
- Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cells are repeatedly exposed to environmental or endogenous stresses that can alter normal cell behavior and increase cell vulnerability. In order to ensure tissue integrity and function, cells cope with cellular injuries by adapting their metabolism, protecting essential intracellular constituents, inhibiting cell death signaling pathways and activating those devoted to damage repair. The molecular chaperones of the heat-shock protein (HSP) family are critical effectors of this adaptive response. They protect intracellular proteins from misfolding or aggregation, inhibit cell death signaling cascades and preserve the intracellular signaling pathways that are essential for cell survival. Most HSPs are rapidly overexpressed in response to cellular injuries including genotoxic stress. DNA damage can dramatically alter cell behavior and contribute to a number of diseases including developmental defects, neurodegenerative disorders, and cancer. Thus, the ability of cells to repair DNA damage is essential for preserving cell integrity. DNA damage activates a coordinated response that includes detecting DNA lesions before their transmission to daughter cells, blocking cell cycle progression and DNA replication and repairing the damage. Although the role of HSPs in proteins homeostasis and cell death, especially apoptosis has been widely reported, much less is known about their function in DNA repair. This review aims to present the role of HSPs in DNA repair signaling pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.