Evidence map›Paper›PMID 28009300›Full record

ArticleCell reports2016

Lineage-Specific and Non-specific Cytokine-Sensing Genes Respond Differentially to the Master Regulator STAT5.

Xianke Zeng, Michaela Willi, Ha Youn Shin, Lothar Hennighausen, Chaochen Wang

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

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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

5 authors at 2 institutions in 2 countries.

Xianke ZengLaboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
Michaela WilliLaboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA; Division of Bioinformatics, Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Ha Youn ShinLaboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
Lothar HennighausenLaboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA. Electronic address: lotharh@mail.nih.gov.
Chaochen WangLaboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA. Electronic address: wangcn@mail.nih.gov.
National Institute of Diabetes and Digestive and Kidney Diseases · USInnsbruck Medical University · AT

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
Genomics Core FacilityZICDK071001 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2023
$16.6M
Intramural NIH HHS Z99 DK999999Intramural NIH HHS ZIA DK061000
6 · The paper itself

Abstract

STAT5, a member of the family of signal transducers and activators of transcription, senses cytokines and controls the biology of cell lineages, including mammary, liver, and T cells. Here, we show that STAT5 activates lineage-specific and widely expressed genes through different mechanisms. STAT5 preferentially binds to promoter sequences of cytokine-responsive genes expressed across cell types and to putative enhancers of lineage-specific genes. While chromatin accessibility of STAT5-based enhancers was dependent on cytokine exposure, STAT5-responsive promoters of widely expressed target genes were generally constitutively accessible. While the contribution of STAT5 to enhancers is well established, its role on promoters is poorly understood. To address this, we focused on Socs2, a widely expressed cytokine-sensing gene. Upon deletion of the STAT5 response elements from the Socs2 promoter in mice, cytokine induction was abrogated, while basal activity remained intact. Our data suggest that promoter-bound STAT5 modulates cytokine responses and enhancer-bound STAT5 is mandatory for gene activation.

Indexed as

3T3 CellsAnimalsBinding SitesCell LineageCytokinesDNA-Binding ProteinsEnhancer Elements, GeneticGene Expression RegulationMicePromoter Regions, GeneticProtein BindingSTAT5 Transcription FactorSuppressor of Cytokine Signaling ProteinsT-LymphocytesTrans-ActivatorsTranscription, GeneticCytokinesDNA-Binding ProteinsSocs2 protein, mouseSTAT5 Transcription FactorSuppressor of Cytokine Signaling ProteinsTrans-Activatorscytokineenhancermammary glandpromoterSOCS2STAT5

Identifiers

PMID28009300
PMCPMC5217531
OpenAlexW2563500270

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.