Evidence map›Paper›PMID 11706048›Full record

ArticleThe Journal of cell biology2001

Signal transducer and activator of transcription (Stat) 5 controls the proliferation and differentiation of mammary alveolar epithelium.

K Miyoshi, J M Shillingford, G H Smith, S L Grimm, K U Wagner, T Oka, J M Rosen, G W Robinson, L Hennighausen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

123 citing papers in PubMed, 275 citations in OpenAlex.

  1. Article
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  5. Mechanisms of Regulation of Cell Fate in Breast Development and Cancer.Advances in experimental medicine and biology · 2025
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63 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

K MiyoshiLaboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. mammary@nih.gov
J M Shillingford
G H Smith
S L Grimm
K U Wagner
T Oka
J M Rosen
G W Robinson
L Hennighausen
National Institute of Diabetes and Digestive and Kidney Diseases · USBaylor College of Medicine · USNational Cancer Institute · USTokushima University · JP

Funding

Genetic Approaches To Understanding Organ Development and FunctionZIADK061000 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HENNIGHAUSEN, LOTHAR · 2009 to 2025
$24.7M
Genetic Understanding Of Organ Development And FunctionZ01DK061000 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HENNIGHAUSEN, LOTHAR · 1998 to 2008
$851k
6 · The paper itself

Abstract

Functional development of mammary epithelium during pregnancy depends on prolactin signaling. However, the underlying molecular and cellular events are not fully understood. We examined the specific contributions of the prolactin receptor (PrlR) and the signal transducers and activators of transcription 5a and 5b (referred to as Stat5) in the formation and differentiation of mammary alveolar epithelium. PrlR- and Stat5-null mammary epithelia were transplanted into wild-type hosts, and pregnancy-mediated development was investigated at a histological and molecular level. Stat5-null mammary epithelium developed ducts but failed to form alveoli, and no milk protein gene expression was observed. In contrast, PrlR-null epithelium formed alveoli-like structures with small open lumina. Electron microscopy revealed undifferentiated features of organelles and a perturbation of cell-cell contacts in PrlR- and Stat5-null epithelia. Expression of NKCC1, an Na-K-Cl cotransporter characteristic for ductal epithelia, and ZO-1, a protein associated with tight junction, were maintained in the alveoli-like structures of PrlR- and Stat5-null epithelia. In contrast, the Na-Pi cotransporter Npt2b, and the gap junction component connexin 32, usually expressed in secretory epithelia, were undetectable in PrlR- and Stat5-null mice. These data demonstrate that signaling via the PrlR and Stat5 is critical for the proliferation and differentiation of mammary alveoli during pregnancy.

Indexed as

Milk ProteinsPregnancy, AnimalAnimalsCell DifferentiationCell DivisionConnexinsDNA-Binding ProteinsEpidermal Growth FactorEpithelial CellsFemaleGap Junction beta-1 ProteinGrowth HormoneMammary Glands, AnimalMiceMice, Inbred C57BLMice, KnockoutConnexinsDNA-Binding ProteinsEpidermal Growth FactorGap Junction beta-1 ProteinGrowth HormoneMilk ProteinsReceptors, ProlactinSlc12a2 protein, mouseSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 2Stat5a protein, mouseSTAT5 Transcription FactorTrans-Activators

Identifiers

PMID11706048
PMCPMC2198867
OpenAlexW2021864884

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.