Evidence map›Paper›PMID 19893491›Full record

ArticleThe EMBO journal2010

CYLD negatively regulates cell-cycle progression by inactivating HDAC6 and increasing the levels of acetylated tubulin.

Sara A Wickström, Katarzyna C Masoumi, Saadi Khochbin, Reinhard Fässler, Ramin Massoumi

Abstract read
In one paragraph

Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
–field-weighted citation impact
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

96 citing papers in PubMed.

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36 more citing papers are in PubMed but not listed here.

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

5 authors.

Sara A WickströmDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Katarzyna C Masoumi
Saadi Khochbin
Reinhard Fässler
Ramin Massoumi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CYLD is a tumour-suppressor gene that is mutated in a benign skin tumour syndrome called cylindromatosis. The CYLD gene product is a deubiquitinating enzyme that was shown to regulate cell proliferation, cell survival and inflammatory responses, mainly through inhibiting NF-kappaB signalling. Here we show that CYLD controls cell growth and division at the G(1)/S-phase as well as cytokinesis by associating with alpha-tubulin and microtubules through its CAP-Gly domains. Translocation of activated CYLD to the perinuclear region of the cell is achieved by an inhibitory interaction of CYLD with histone deacetylase-6 (HDAC6) leading to an increase in the levels of acetylated alpha-tubulin around the nucleus. This facilitates the interaction of CYLD with Bcl-3, leading to a significant delay in the G(1)-to-S-phase transition. Finally, CYLD also interacts with HDAC6 in the midbody where it regulates the rate of cytokinesis in a deubiquitinase-independent manner. Altogether these results identify a mechanism by which CYLD regulates cell proliferation at distinct cell-cycle phases.

Indexed as

AcetylationAnimalsCarcinoma, Adenoid CysticCatalytic DomainCell CycleCell Line, TumorCytokinesisDeubiquitinating Enzyme CYLDGenes, Tumor SuppressorHistone Deacetylase 6Histone DeacetylasesHumansKeratinocytesMelanocytesMelanomaMiceCYLD protein, humanDeubiquitinating Enzyme CYLDHDAC6 protein, humanHistone Deacetylase 6Histone DeacetylasesRecombinant Fusion ProteinsTetradecanoylphorbol AcetateTubulinTumor Suppressor Proteins

Identifiers

PMID19893491
PMCPMC2775896

What OpenQuestion holds

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Read underepoch 390

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.