Evidence map›Paper›PMID 15485906›Full record

ArticleMolecular and cellular biology2004

Cofilin 1 is revealed as an inhibitor of glucocorticoid receptor by analysis of hormone-resistant cells.

Joëlle Rüegg, Florian Holsboer, Christoph Turck, Theo Rein

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. The Stress-Inducible Protein DRR1 Exerts Distinct Effects on Actin Dynamics.International journal of molecular sciences · 2018
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  9. Aberrant expression of c-Jun in glioblastoma by internal ribosome entry site (IRES)-mediated translational activation.Proceedings of the National Academy of Sciences of the United States of America · 2012
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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

4 authors at 2 institutions in 1 country.

Joëlle RüeggMax Planck Institute of Psychiatry, Kraepelinstr. 10, D-80804 Munich, Germany.
Florian Holsboer
Christoph Turck
Theo Rein
Max Planck Society · DEMax Planck Institute of Psychiatry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Significant knowledge about glucocorticoid signaling has accumulated, yet many aspects remain unknown. We aimed to discover novel factors involved in glucocorticoid receptor regulation that do not necessarily require direct receptor interaction. We achieved this by using a functional genetic screen: a stable cell line which cannot survive hormone treatment was engineered, randomly mutated, and selected in the presence of glucocorticoid. A hormone-resistant clone was analyzed by two-dimensional gel electrophoresis. Differentially expressed proteins were identified and tested as candidates for regulation of the glucocorticoid receptor. An unexpected candidate, cofilin 1, inhibited receptor activity. Cofilin is known to promote actin depolymerization and filament severing. Several experiments suggest that this feature of cofilin is involved in its inhibitory action. Both its actin depolymerization activity and its inhibitory action on the receptor are dependent on its phosphorylation state. Treatment of cells with a cytoskeleton-disrupting agent decreased receptor activity, as did overexpression of actin, particularly a mutant actin that does not polymerize. In addition, overexpression of cofilin and actin as well as chemical cytoskeleton disruption changed the subcellular receptor distribution and upregulated c-Jun, which could constitute the inhibitory mechanism of cofilin. In summary, cofilin represents a novel factor that can cause glucocorticoid resistance.

Indexed as

Drug ResistanceActin Depolymerizing FactorsActinsBiopolymersCell LineCell NucleusElectrophoresis, Gel, Two-DimensionalGene ExpressionGlucocorticoidsHumansMicrofilament ProteinsMutagenesisMutationPhenotypePhosphorylationProtein TransportActin Depolymerizing FactorsActinsBiopolymersGlucocorticoidsMicrofilament ProteinsProto-Oncogene Proteins c-junReceptors, GlucocorticoidThioredoxins

Identifiers

PMID15485906
PMCPMC522229
OpenAlexW2134148114

What OpenQuestion holds

Textmetadata
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.