Evidence map›Paper›PMID 21628546›Full record

ArticleJournal of biological rhythms2011

Modulation of clock gene expression by the transcriptional coregulator receptor interacting protein 140 (RIP140).

Ariel H B Poliandri, Joshua J Gamsby, Mark Christian, Michael J Spinella, Jennifer J Loros, Jay C Dunlap, Malcolm G Parker

Open access · hybridAbstract read
In one paragraph

Article in Journal of biological rhythms, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Deletion of Nrip1 Extends Female Mice Longevity, Increases Autophagy, and Delays Cell Senescence.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018
    Article
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  7. Review
  8. Article
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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

7 authors at 2 institutions in 2 countries.

Ariel H B PoliandriInstitute of Reproductive and Developmental Biology, Faculty of Medicine, Imperial College London, London, United Kingdom.
Joshua J Gamsby
Mark Christian
Michael J Spinella
Jennifer J Loros
Jay C Dunlap
Malcolm G Parker
Dartmouth–Hitchcock Medical Center · USImperial College London · GB

Funding

Identification and Analysis of Circadian Clock-Controlled GenesR01GM083336 · NIGMS · DARTMOUTH COLLEGE · PI LOROS, JENNIFER J. · 2008 to 2015
$5.7M
Biotechnology and Biological Sciences Research Council BB/C504327/1NIGMS NIH HHS R01 GM083336Wellcome Trust 079200/Z/06/Z
6 · The paper itself

Abstract

Circadian rhythms are generated in central and peripheral tissues by an intracellular oscillating timing mechanism known as the circadian clock. Several lines of evidence show a strong and bidirectional interplay between metabolism and circadian rhythms. Receptor interacting protein 140 (RIP140) is a coregulator for nuclear receptors and other transcription factors that represses catabolic pathways in metabolic tissues. Although RIP140 functions as a corepressor for most nuclear receptors, mounting evidence points to RIP140 as a dual coregulator that can repress or activate different sets of genes. Here, we demonstrate that RIP140 mRNA and protein levels are under circadian regulation and identify RIP140 as a modulator of clock gene expression, suggesting that RIP140 can participate in a feedback mechanism affecting the circadian clock. We show that the absence of RIP140 disturbs the basal levels of BMAL1 and other clock genes, reducing the amplitude of their oscillations. In addition, we demonstrate that RIP140 is recruited to retinoid-related orphan receptor (ROR) binding sites on the BMAL1 promoter, directly interacts with RORα, and increases transcription from the BMAL1 promoter in a RORα-dependent manner. These results indicate that RIP140 is not only involved in metabolic control but also acts as a coactivator for RORα, influencing clock gene expression.

Indexed as

Circadian RhythmGene Expression RegulationAdaptor Proteins, Signal TransducingAnimalsARNTL Transcription FactorsCells, CulturedCircadian ClocksFibroblastsMaleMiceMice, Inbred C57BLNuclear ProteinsNuclear Receptor Interacting Protein 1Nuclear Receptor Subfamily 1, Group F, Member 1RNA, MessengerAdaptor Proteins, Signal TransducingARNTL Transcription FactorsBmal1 protein, mouseNuclear ProteinsNuclear Receptor Interacting Protein 1Nuclear Receptor Subfamily 1, Group F, Member 1RNA, MessengerRora protein, mouse

Identifiers

PMID21628546
PMCPMC3207295
OpenAlexW2161660591

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.