Evidence map›Paper›PMID 25360623›Full record

ArticlePloS one2014

Hormonal induction and roles of Disabled-2 in lactation and involution.

Wensi Tao, Robert Moore, Elizabeth R Smith, Xiang-Xi Xu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice.Frontiers in cell and developmental biology · 2016
    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

4 authors at 2 institutions in 1 country.

Wensi TaoSylvester Comprehensive Cancer Center, and Department of Cell Biology, Graduate Program in Molecular Cell and Developmental Biology, University of Miami Miller School of Medicine, Miami, Florida, United States of America.
Robert MooreSylvester Comprehensive Cancer Center, and Department of Cell Biology, Graduate Program in Molecular Cell and Developmental Biology, University of Miami Miller School of Medicine, Miami, Florida, United States of America.
Elizabeth R SmithSylvester Comprehensive Cancer Center, and Department of Cell Biology, Graduate Program in Molecular Cell and Developmental Biology, University of Miami Miller School of Medicine, Miami, Florida, United States of America.
Xiang-Xi XuSylvester Comprehensive Cancer Center, and Department of Cell Biology, Graduate Program in Molecular Cell and Developmental Biology, University of Miami Miller School of Medicine, Miami, Florida, United States of America.
University of Miami · USSylvester Comprehensive Cancer Center · US

Funding

Ovarian Cancer: Epithelial DedifferentiationR01CA079716 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI XU, XIANGXI MIKE · 1999 to 2015
$4.8M
Epithelial Positioning Organization and Ovarian CancerR01CA095071 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI XU, XIANGXI MIKE · 2002 to 2010
$3.2M
DAB2 AND RAS REGULATIONR01CA075389 · NCI · INSTITUTE FOR CANCER RESEARCH · PI XU, XIANGXI MIKE · 1997 to 2001
$534k
NCI NIH HHS CA75389NCI NIH HHS CA79716NCI NIH HHS R01 CA079716NCI NIH HHS R01 CA095071
6 · The paper itself

Abstract

Disabled-2 (Dab2) is a widely expressed endocytic adaptor that was first isolated as a 96 KDa phospho-protein, p96, involved in MAPK signal transduction. Dab2 expression is lost in several cancer types including breast cancer, and Dab2 is thought to have a tumor suppressor function. In mammary epithelia, Dab2 was induced upon pregnancy and further elevated during lactation. We constructed mutant mice with a mosaic Dab2 gene deletion to bypass early embryonic lethality and to investigate the roles of Dab2 in mammary physiology. Loss of Dab2 had subtle effects on lactation, but Dab2-deficient mammary glands showed a strikingly delayed cell clearance during involution. In primary cultures of mouse mammary epithelial cells, Dab2 proteins were also induced by estrogen, progesterone, and/or prolactin. Dab2 null mammary epithelial cells were refractory to growth suppression induced by TGF-beta. However, Dab2 deletion did not affect Smad2 phosphorylation; rather TGF-beta-stimulated MAPK activation was enhanced in Dab2-deficient cells. We conclude that Dab2 expression is induced by hormones and Dab2 plays a role in modulating TGF-beta signaling to enhance apoptotic clearance of mammary epithelial cells during involution.

Indexed as

LactationAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportAnimalsApoptosis Regulatory ProteinsCell ProliferationEpithelial CellsFemaleGene Expression RegulationGene Knockout TechniquesHormonesMammary Glands, AnimalMiceOrgan SizePregnancyReproductionAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportApoptosis Regulatory ProteinsDab2 protein, mouseHormones

Identifiers

PMID25360623
PMCPMC4216001
OpenAlexW2079020661

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.