Evidence map›Paper›PMID 21038417›Full record

ArticleHepatology (Baltimore, Md.)2010

The transcription factors signal transducer and activator of transcription 5A (STAT5A) and STAT5B negatively regulate cell proliferation through the activation of cyclin-dependent kinase inhibitor 2b (Cdkn2b) and Cdkn1a expression.

Ji Hoon Yu, Bing-Mei Zhu, Mark Wickre, Gregory Riedlinger, Weiping Chen, Atsushi Hosui, Gertraud W Robinson, Lothar Hennighausen

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Growth hormone and nonalcoholic fatty liver disease.Immunometabolism (Cobham, Surrey) · 2023 · on this map
    Review
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  19. Review
  20. MicroRNA and transcription factor mediated regulatory network for ovarian cancer: regulatory network of ovarian cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
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.

Ji Hoon YuLaboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Bing-Mei Zhu
Mark Wickre
Gregory Riedlinger
Weiping Chen
Atsushi Hosui
Gertraud W Robinson
Lothar Hennighausen
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · USOsaka 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
Intramural NIH HHS Z01 DK061000
6 · The paper itself

Abstract

unlabelledAlthough the cytokine-inducible transcription factor signal transducer and activator of transcription 5 (STAT5) promotes proliferation of a wide range of cell types, there are cell-specific and context-specific cases in which loss of STAT5 results in enhanced cell proliferation. Here, we report that loss of STAT5 from mouse embryonic fibroblasts (MEFs) leads to enhanced proliferation, which was linked to reduced levels of the cell cycle inhibitors p15(INK4B) and p21(CIP1). We further demonstrate that growth hormone, through the transcription factor STAT5, enhances expression of the Cdkn2b (cyclin-dependent kinase inhibitor 2B) gene and that STAT5A binds to interferon-gamma-activated sequence sites within the promoter. We recently demonstrated that ablation of STAT5 from liver results in hepatocellular carcinoma upon CCl₄ treatment. We now establish that STAT5, like in MEFs, activates expression of the Cdkn2b gene in liver tissue. Loss of STAT5 led to diminished p15(INK4B) and increased hepatocyte proliferation.

conclusionThis study for the first time demonstrates that cytokines, through STAT5, induce the expression of a key cell cycle inhibitor. These experiments therefore shed mechanistic light on the context-specific role of STAT5 as tumor suppressor.

Indexed as

AnimalsCarbon TetrachlorideCarcinoma, HepatocellularCell CycleCell DivisionCyclin-Dependent Kinase Inhibitor p19Cyclin-Dependent Kinase Inhibitor p21Embryo, MammalianFibroblastsHomeostasisLiver CirrhosisLiver NeoplasmsMaleMiceMice, KnockoutMice, TransgenicCarbon TetrachlorideCdkn1a protein, mouseCdkn2d protein, mouseCyclin-Dependent Kinase Inhibitor p19Cyclin-Dependent Kinase Inhibitor p21Stat5a protein, mouseStat5b protein, mouseSTAT5 Transcription FactorTumor Suppressor Proteins

Identifiers

PMID21038417
PMCPMC3152209
OpenAlexW2065145360

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.