Evidence map›Paper›PMID 21840410›Full record

ReviewSeminars in cell & developmental biology2011

Mediator and human disease.

Jason M Spaeth, Nam Hee Kim, Thomas G Boyer

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

53 citing papers in PubMed, 92 citations in OpenAlex.

  1. Heterozygous Med13l mice recapitulate a developmental growth delay and craniofacial anomalies seen in MED13L syndrome.Developmental dynamics : an official publication of the American Association of Anatomists · 2026
    Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Novel insights into the phenotypic spectrum and pathogenesis of Hardikar syndrome.Genetics in medicine : official journal of the American College of Medical Genetics · 2024
    Article
  8. Article
  9. Genetically Engineered Mice Unveil In Vivo Roles of the Mediator Complex.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. CDK19-related disorder results from both loss-of-function and gain-of-function de novo missense variants.Genetics in medicine : official journal of the American College of Medical Genetics · 2021
    Article
  14. Genes · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Twenty years of Mediator complex structural studies.Biochemical Society transactions · 2019
    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.

Jason M SpaethDepartment of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78245, USA.
Nam Hee Kim
Thomas G Boyer
The University of Texas Health Science Center at San Antonio · US

Funding

Mediator and epigenetic control of neuronal gene expression and differentiationR01MH085320 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BOYER, THOMAS G · 2009 to 2013
$1.8M
Osteoblast differentiation: Interactions of Wnt, Runx2 and FGFR01AR053100 · NIAMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BOYER, THOMAS G · 2008 to 2012
$1.4M
NIAMS NIH HHS AR053100NIAMS NIH HHS R01 AR053100NIMH NIH HHS MH085320NIMH NIH HHS R01 MH085320
6 · The paper itself

Abstract

Since the identification of a metazoan counterpart to yeast Mediator nearly 15 years ago, a convergent body of biochemical and molecular genetic studies have confirmed their structural and functional relationship as an integrative hub through which regulatory information conveyed by signal activated transcription factors is transduced to RNA polymerase II. Nonetheless, metazoan Mediator complexes have been shaped during evolution by substantive diversification and expansion in both the number and sequence of their constituent subunits, with important implications for the development of multicellular organisms. The appearance of unique interaction surfaces within metazoan Mediator complexes for transcription factors of diverse species-specific origins extended the role of Mediator to include an essential function in coupling developmentally coded signals with precise gene expression output sufficient to specify cell fate and function. The biological significance of Mediator in human development, suggested by genetic studies in lower metazoans, is emphatically illustrated by an expanding list of human pathologies linked to genetic variation or aberrant expression of its individual subunits. Here, we review our current body of knowledge concerning associations between individual Mediator subunits and specific pathological disorders. When established, molecular etiologies underlying genotype-phenotype correlations are addressed, and we anticipate that future progress in this critical area will help identify therapeutic targets across a range of human pathologies.

Indexed as

Cardiovascular DiseasesFemaleGene Expression RegulationHumansMaleMediator ComplexMental DisordersNeoplasmsNeoplasms, Hormone-DependentNervous System DiseasesProtein SubunitsRNA Polymerase IISignal TransductionTranscription FactorsMediator ComplexProtein SubunitsRNA Polymerase IITranscription Factors

Identifiers

PMID21840410
PMCPMC4100472
OpenAlexW2050342734

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.