Evidence map›Paper›PMID 26044764›Full record

ArticleScientific reports2015

Gradual reduction in rRNA transcription triggers p53 acetylation and apoptosis via MYBBP1A.

Takuya Kumazawa, Kazuho Nishimura, Naohiro Katagiri, Sayaka Hashimoto, Yuki Hayashi, Keiji Kimura

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Takuya Kumazawa1] Graduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennnoudai, Tsukuba 305-8577, Japan [2] First Department of Internal Medicine, Nara Medical University, 840 Shijo-cho Kashihara, Nara 634-8522, Japan.
Kazuho NishimuraGraduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennnoudai, Tsukuba 305-8577, Japan.
Naohiro KatagiriGraduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennnoudai, Tsukuba 305-8577, Japan.
Sayaka HashimotoGraduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennnoudai, Tsukuba 305-8577, Japan.
Yuki HayashiGraduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennnoudai, Tsukuba 305-8577, Japan.
Keiji KimuraGraduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennnoudai, Tsukuba 305-8577, Japan.
University of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nucleolus, whose primary function is ribosome biogenesis, plays an essential role in p53 activation. Ribosome biogenesis is inhibited in response to cellular stress and several nucleolar proteins translocate from the nucleolus to the nucleoplasm, where they activate p53. In this study, we analysed precisely how impaired ribosome biogenesis regulates the activation of p53 by depleting nucleolar factors involved in rRNA transcription or rRNA processing. Nucleolar RNA content decreased when rRNA transcription was inhibited. In parallel with the reduced levels of nucleolar RNA content, the nucleolar protein Myb-binding protein 1 A (MYBBP1A) translocated to the nucleoplasm and increased p53 acetylation. The acetylated p53 enhanced p21 and BAX expression and induced apoptosis. In contrast, when rRNA processing was inhibited, MYBBP1A remained in the nucleolus and nonacetylated p53 accumulated, causing cell cycle arrest at the G1 phase by inducing p21 but not BAX. We propose that the nucleolus functions as a stress sensor to modulate p53 protein levels and its acetylation status, determining cell fate between cell cycle arrest and apoptosis by regulating MYBBP1A translocation.

Indexed as

Transcription, GeneticAcetylationApoptosisCell Line, TumorCell NucleusDNA-Binding ProteinsG1 Phase Cell Cycle CheckpointsHumansModels, BiologicalNuclear ProteinsNucleocytoplasmic Transport ProteinsProtein TransportRibosomal ProteinsRNA-Binding ProteinsRNA InterferenceRNA, RibosomalDNA-Binding ProteinsMYBBP1A protein, humanNuclear ProteinsNucleocytoplasmic Transport Proteinsribosomal protein L11Ribosomal ProteinsRNA-Binding ProteinsRNA, RibosomalTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID26044764
PMCPMC4456663
OpenAlexW1891788086

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Registered trials

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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.