Evidence map›Paper›PMID 21247416›Full record

ArticleBMC genomics2011

Ubiquitin-proteasome genes as targets for modulation of cisplatin sensitivity in fission yeast.

Laura Gatti, Kwang L Hoe, Jacqueline Hayles, Sabina C Righetti, Nives Carenini, Laura Dal Bo, Dong U Kim, Han O Park, Paola Perego

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. PLAA/UFD-3 regulates P-bodies through its intrinsic disordered domain.Proceedings of the National Academy of Sciences of the United States of America · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Laura GattiFondazione IRCCS, Istituto Nazionale per Studio e Cura dei Tumori, 20133 Milan, Italy.
Kwang L Hoe
Jacqueline Hayles
Sabina C Righetti
Nives Carenini
Laura Dal Bo
Dong U Kim
Han O Park
Paola Perego
Fondazione IRCCS Istituto Nazionale dei Tumori · ITKorea Research Institute of Bioscience and Biotechnology · KRCancer Research UK · GB

Funding

Wellcome Trust 093917
6 · The paper itself

Abstract

backgroundThe ubiquitin(Ub)-proteasome pathway is implicated in the regulation of a variety of cellular functions and plays a major role in stress response in eukaryotic cells, by targeting misfolded and damaged proteins for degradation. In addition, in the presence of DNA damage, the Ub-proteasome system regulates proteins involved in sensing, repairing, and/or tolerating the damage. Antitumor agents such as cisplatin can activate the pathway, but the role of specific pathway components in cell sensitivity/response to the drug is not known. Since platinum compounds represent clinically relevant antitumor agents and a major limitation to their use is the development of drug resistance, there is an urgent need for identifying targets for improving their efficacy.

resultsIn the present study, we performed a genome-wide screening for sensitivity to cisplatin using non-essential haploid deletion mutants of the fission yeast Schizosaccharomyces pombe, belonging to a collection of haploid strains constructed through homologous recombination. Using this approach, we identified three Ub-proteasome mutants exhibiting hypersensitivity to cisplatin (ubp16, ubc13 and pmt3) and ten mutants (including ufd2, beta7 20S, rpt6/let1) resistant to the drug. In addition, the importance of lub1 gene emerged from the comparison between the present screening and gene expression profile data previously obtained in fission yeast.

conclusionsThe factors identified in the present study allowed us to highlight most finely the close relationship between the Ub-proteasome system and DNA damage response mechanisms, thus establishing a comprehensive framework of regulators likely relevant also in higher eukaryotes. Our results provide the proof of principle of the involvement of specific genes modulated by cisplatin treatment in cell response to the drug, suggesting their potential role as targets for modulating cisplatin sensitivity. In this regard, the prospective identification of novel targets for modulation of cisplatin sensitivity in an eukaryotic model organism appears particularly intriguing towards the discovery of strategies to overcome cisplatin resistance in human tumors.

Indexed as

CisplatinProteasome Endopeptidase ComplexRepressor ProteinsSchizosaccharomycesSchizosaccharomyces pombe ProteinsUbiquitinUbiquitin-Conjugating EnzymesCisplatinPmt3 protein, S pombeProteasome Endopeptidase ComplexRepressor ProteinsSchizosaccharomyces pombe ProteinsUbc13 protein, S pombeUbiquitinUbiquitin-Conjugating Enzymes

Identifiers

PMID21247416
PMCPMC3032702
OpenAlexW2032344198

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.