Evidence map›Paper›PMID 20351249›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Key roles for MED1 LxxLL motifs in pubertal mammary gland development and luminal-cell differentiation.

Pingping Jiang, Qiuping Hu, Mitsuhiro Ito, Sara Meyer, Susan Waltz, Sohaib Khan, Robert G Roeder, Xiaoting Zhang

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
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  6. Article
  7. Characterization ofToxins · 2023
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  14. Article
  15. Article
  16. Transcriptional Regulation of Dental Epithelial Cell Fate.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Article
  19. Review
  20. Understanding Obesity as a Risk Factor for Uterine Tumors Using Drosophila.Advances in experimental medicine and biology · 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

8 authors at 3 institutions in 2 countries.

Pingping JiangDepartment of Cancer and Cell Biology, College of Medicine, University of Cincinnati, 3125 Eden Avenue, OH 45267, USA.
Qiuping Hu
Mitsuhiro Ito
Sara Meyer
Susan Waltz
Sohaib Khan
Robert G Roeder
Xiaoting Zhang
University of Cincinnati · USRockefeller University · USZhejiang University · CN

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2007 to 2026
$24.4M
Nuclear Receptor Coactivator Functions and MechanismsR01DK071900 · NIDDK · ROCKEFELLER UNIVERSITY · PI ROEDER, ROBERT G · 2005 to 2015
$5.9M
The Ron Receptor in Mammary Gland BiologyR01CA100002 · NCI · UNIVERSITY OF CINCINNATI · PI WALTZ, SUSAN E · 2004 to 2008
$1.5M
NCI NIH HHS CA100002NCI NIH HHS R01 CA100002NIDDK NIH HHS DK071900NIDDK NIH HHS P30 DK078392NIDDK NIH HHS R01 DK071900
6 · The paper itself

Abstract

Mediator recently has emerged as a central player in the direct transduction of signals from transcription factors to the general transcriptional machinery. In the case of nuclear receptors, in vitro studies have shown that the transcriptional coactivator function of the Mediator involves direct ligand-dependent interactions of the MED1 subunit, through its two classical LxxLL motifs, with the receptor AF2 domain. However, despite the strong in vitro evidence, there currently is little information regarding in vivo functions of the LxxLL motifs either in MED1 or in other coactivators. Toward this end, we have generated MED1 LxxLL motif-mutant knockin mice. Interestingly, these mice are both viable and fertile and do not exhibit any apparent gross abnormalities. However, they do exhibit severe defects in pubertal mammary gland development. Consistent with this phenotype, as well as loss of the strong ligand-dependent estrogen receptor (ER)alpha-Mediator interaction, expression of a number of known ERalpha-regulated genes was down-regulated in MED1-mutant mammary epithelial cells and could no longer respond to estrogen stimulation. Related, estrogen-stimulated mammary duct growth in MED1-mutant mice was also greatly diminished. Finally, additional studies show that MED1 is differentially expressed in different types of mammary epithelial cells and that its LxxLL motifs play a role in mammary luminal epithelial cell differentiation and progenitor/stem cell determination. Our results establish a key nuclear receptor- and cell-specific in vivo role for MED1 LxxLL motifs, through Mediator-ERalpha interactions, in mammary gland development.

Indexed as

Amino Acid MotifsAnimalsCell DifferentiationCell NucleusCell SeparationEstrogen Receptor alphaEstrogensFlow CytometryLigandsMammary Glands, AnimalMediator Complex Subunit 1MiceMice, Inbred C57BLStem CellsEstrogen Receptor alphaEstrogensLigandsMed1 protein, mouseMediator Complex Subunit 1

Identifiers

PMID20351249
PMCPMC2872411
OpenAlexW1974527727

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.