Evidence map›Paper›PMID 21737676›Full record

ArticleMolecular biology of the cell2011

The role of RelA (p65) threonine 505 phosphorylation in the regulation of cell growth, survival, and migration.

Aichi Msaki, Ana M Sánchez, Li Fang Koh, Benjamin Barré, Sonia Rocha, Neil D Perkins, Renée F Johnson

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024
    Review
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  16. Review
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  18. Review
  19. The importance of the p50 NF-κB subunit.Cell cycle (Georgetown, Tex.) · 2015
    Article
  20. IKK phosphorylates RelB to modulate its promoter specificity and promote fibroblast migration downstream of TNF receptors.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
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

7 authors at 3 institutions in 2 countries.

Aichi MsakiWellcome Trust Centre for Gene Regulation and Expression, University of Dundee, Dundee DD1 5EH, United Kingdom.
Ana M Sánchez
Li Fang Koh
Benjamin Barré
Sonia Rocha
Neil D Perkins
Renée F Johnson
Newcastle University · GBUniversity of Dundee · GBUniversité d'Angers · FR

Funding

Cancer Research UK 12750Cancer Research UK 12918Wellcome Trust 083524Worldwide Cancer Research 08-0430
6 · The paper itself

Abstract

The NF-κB family of transcription factors is a well-established regulator of the immune and inflammatory responses and also plays a key role in other cellular processes, including cell death, proliferation, and migration. Conserved residues in the trans-activation domain of RelA, which can be posttranslationally modified, regulate divergent NF-κB functions in response to different cellular stimuli. Using rela(-/-) mouse embryonic fibroblasts reconstituted with RelA, we find that mutation of the threonine 505 (T505) phospho site to alanine has wide-ranging effects on NF-κB function. These include previously described effects on chemotherapeutic drug-induced apoptosis, as well as new roles for this modification in autophagy, cell proliferation, and migration. This last effect was associated with alterations in the actin cytoskeleton and expression of cellular migration-associated genes such as WAVE3 and α-actinin 4. We also define a new component of cisplatin-induced, RelA T505-dependent apoptosis, involving induction of NOXA gene expression, an effect explained at least in part through induction of the p53 homologue, p73. Therefore, in contrast to other RelA phosphorylation events, which positively regulate NF-κB function, we identified RelA T505 phosphorylation as a negative regulator of its ability to induce diverse cellular processes such as apoptosis, autophagy, proliferation, and migration.

Indexed as

Cell MovementCell ProliferationCell SurvivalActin CytoskeletonActininAnimalsAntineoplastic AgentsApoptosisbcl-X ProteinCell LineCisplatinFibroblastsGene ExpressionGene Expression RegulationGene Knockout TechniquesMiceActininAntineoplastic AgentsBcl2l1 protein, mousebcl-X ProteinCisplatinPmaip1 protein, mouseProto-Oncogene Proteins c-bcl-2Rela protein, mouseThreonineTranscription Factor RelATumor Necrosis Factor-alphaWasf3 protein, mouseWiskott-Aldrich Syndrome Protein Family

Identifiers

PMID21737676
PMCPMC3164452
OpenAlexW2157350623

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.