Evidence map›Paper›PMID 15988019›Full record

ArticleMolecular and cellular biology2005

Dysregulation of the peroxisome proliferator-activated receptor target genes by XPD mutations.

Emmanuel Compe, Pascal Drané, Camille Laurent, Karin Diderich, Cathy Braun, Jan H J Hoeijmakers, Jean-Marc Egly

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 136 citations in OpenAlex.

  1. Article
  2. Review
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  6. Review
  7. Nuclear Receptors and Lipid Sensing.Advances in experimental medicine and biology · 2022
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  8. Review
  9. Thyroid hormone receptor phosphorylation regulates acute fasting-induced suppression of the hypothalamic-pituitary-thyroid axis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Reduced levels of prostaglandin IProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Article
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  14. CDK7 inhibitors as anticancer drugs.Cancer metastasis reviews · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Functional Regulation of PPARs through Post-Translational Modifications.International journal of molecular sciences · 2018
    Review
  19. Review
  20. Article

1 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

7 authors at 2 institutions in 2 countries.

Emmanuel CompeInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch Cedex, CU Strasbourg, France.
Pascal Drané
Camille Laurent
Karin Diderich
Cathy Braun
Jan H J Hoeijmakers
Jean-Marc Egly
Institut de génétique et de biologie moléculaire et cellulaire · FRErasmus University Rotterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the XPD subunit of TFIIH give rise to human genetic disorders initially defined as DNA repair syndromes. Nevertheless, xeroderma pigmentosum (XP) group D (XP-D) patients develop clinical features such as hypoplasia of the adipose tissue, implying a putative transcriptional defect. Knowing that peroxisome proliferator-activated receptors (PPARs) are implicated in lipid metabolism, we investigated the expression of PPAR target genes in the adipose tissues and the livers of XPD-deficient mice and found that (i) some genes are abnormally overexpressed in a ligand-independent manner which parallels an increase in the recruitment of RNA polymerase (pol) II but not PPARs on their promoter and (ii) upon treatment with PPAR ligands, other genes are much less induced compared to the wild type, which is due to a lower recruitment of both PPARs and RNA pol II. The defect in transactivation by PPARs is likely attributable to their weaker phosphorylation by the cdk7 kinase of TFIIH. Having identified the phosphorylated residues in PPAR isotypes, we demonstrate how their transactivation defect in XPD-deficient cells can be circumvented by overexpression of either a wild-type XPD or a constitutively phosphorylated PPAR S/E. This work emphasizes that underphosphorylation of PPARs affects their transactivation and consequently the expression of PPAR target genes, thus contributing in part to the XP-D phenotype.

Indexed as

Adipose TissueAnimalsDNA-Binding ProteinsDNA HelicasesLiverMiceMice, Mutant StrainsMutationPhosphorylationPPAR alphaPPAR gammaRNA, MessengerTranscriptional ActivationTranscription FactorsTranscription Factors, TFIITranscription Factor TFIIHDNA-Binding ProteinsDNA HelicasesErcc2 protein, mousePPAR alphaPPAR gammaRNA, MessengerTranscription FactorsTranscription Factors, TFIITranscription Factor TFIIHXeroderma Pigmentosum Group D Protein

Identifiers

PMID15988019
PMCPMC1168804
OpenAlexW2141835372

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.