Evidence map›Paper›PMID 22018181›Full record

ReviewClinical and experimental rheumatology

Glucocorticoid receptor: implications for rheumatic diseases.

T Kino, E Charmandari, G P Chrousos

Abstract readReview
In one paragraph

Review in Clinical and experimental rheumatology. 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
2.1field-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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
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  9. Review
  10. Article
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  13. Chronopharmacology of glucocorticoids.Advanced drug delivery reviews
    Review
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

3 authors at 1 institution in 1 country.

T KinoEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. kinot@mail.nih.gov
E Charmandari
G P Chrousos
Eunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Molecular Mediators and Regulators of Glucocorticoid ActionsZIAHD008732 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI KINO, TOMOSHIGE · 2009 to 2014
$5.1M
Endocrine-immune-reproductive System InteractionsZIAHD000615 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI KINO, TOMOSHIGE · 2009 to 2014
$2.0M
Pathophysiology of The Hypothalamic-pituitary-adrenal & Gonadal AxesZIAHD000618 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI KINO, TOMOSHIGE · 2009 to 2014
$2.0M
PHYSIOLOGY &PATHOPHYSIOLOGY OF THE HYPOTHALAMIC-PITUITARY-ADRENAL &GONADAL AXEZ01HD000618 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI KINO, TOMOSHIGE · 1985 to 2008
$584k
Intramural NIH HHS Z01 HD000618Intramural NIH HHS ZIA HD008732
6 · The paper itself

Abstract

The glucocorticoid receptor (GR), a member of the nuclear receptor superfamily, mediates most of the known biologic effects of glucocorticoids. The human GR gene consists of 9 exons and expresses 2 alternative splicing isoforms, the GRα and GRβ. GRα is the classic receptor that binds to glucocorticoids and mediates most of the known actions of glucocorticoids, while GRβ does not bind to these hormones and exerts a dominant negative effect upon the GRα-induced transcriptional activity. Each of the two GR splice isoforms has 8 translational variants with specific transcriptional activity and tissue distribution. GRα consists of three subdomains, translocates from the cytoplasm into the nucleus upon binding to glucocorticoids, and regulates the transcriptional activity of numerous glucocorticoid-responsive genes either by binding to its cognate DNA sequences or by interacting with other transcription factors. In addition to these genomic actions, the GR also exerts rapid, non-genomic effects, which are possibly mediated by membrane-localised receptors or by translocation into the mitochondria. All these actions of the GR appear to play an important role in the regulation of the immune system. Specifically, the splicing variant GRβ may be involved in the pathogenesis of rheumatic diseases, while the circadian regulation of the GR activity via acetylation by the Clock transcription factor may have therapeutic implications for the preferential timing of glucocorticoid administration in autoimmune inflammatory disorders.

Indexed as

HumansIsomerismProtein Structure, TertiaryReceptors, GlucocorticoidRheumatic DiseasesTranscriptional ActivationReceptors, Glucocorticoid

Identifiers

PMID22018181
PMCPMC3630375
OpenAlexW71521485

What OpenQuestion holds

Textmetadata
LicenceTDM
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.