Evidence map›Paper›PMID 28003426›Full record

ArticleMolecular pharmacology2017

Pyruvate Dehydrogenase Kinase 4 Deficiency Results in Expedited Cellular Proliferation through E2F1-Mediated Increase of Cyclins.

Jonathan Choiniere, Jianguo Wu, Li Wang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-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

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  4. Cancer biology & therapy · 2023
    Article
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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

3 authors at 1 institution in 2 countries.

Jonathan ChoiniereDepartment of Physiology and Neurobiology, Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut (J.C., J.W., L.W.); Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut (L.W.); Section of Digestive Diseases, Department of Internal Medicine, Yale University, New Haven, Connecticut (L.W.); and School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China (L.W.).
Jianguo WuDepartment of Physiology and Neurobiology, Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut (J.C., J.W., L.W.); Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut (L.W.); Section of Digestive Diseases, Department of Internal Medicine, Yale University, New Haven, Connecticut (L.W.); and School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China (L.W.).
Li WangDepartment of Physiology and Neurobiology, Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut (J.C., J.W., L.W.); Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut (L.W.); Section of Digestive Diseases, Department of Internal Medicine, Yale University, New Haven, Connecticut (L.W.); and School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China (L.W.) li.wang@uconn.edu.
Yale University · US

Funding

Yale Liver CenterP30DK034989 · NIDDK · YALE UNIVERSITY · PI WAJAHAT Zafar MEHAL · 1986 to 2026
$31.1M
SHP-regulation of Lipid and Lipoprotein MetabolismR01DK080440 · NIDDK · UNIVERSITY OF UTAH · PI WANG, LI · 2008 to 2015
$2.3M
LncRNA as a New Mediator of Bile Acid HomeostasisR01DK104656 · NIDDK · UNIVERSITY OF CONNECTICUT STORRS · PI WANG, LI · 2015 to 2018
$1.7M
Molecular Basis of Cancer Cell Metabolic ReprogrammingR01ES025909 · NIEHS · UNIVERSITY OF CONNECTICUT STORRS · PI WANG, LI · 2015 to 2017
$1.0M
Long noncoding RNAs in alcoholic liver diseaseR21AA024935 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI LIANGPUNSAKUL, SUTHAT, WANG, LI · 2016 to 2017
$431k
Alcohol, nuclear receptor signaling, and circadian clocksR21AA022482 · NIAAA · UNIVERSITY OF CONNECTICUT STORRS · PI WANG, LI · 2015 to 2016
$415k
Circadian Clock Regulation of Alcoholic Liver DiseaseI01BX002634 · VA · VA CONNECTICUT HEALTHCARE SYSTEM · PI WANG, LI · 2016 to 2019
–
BLRD VA I01 BX002634NIAAA NIH HHS R21 AA022482NIAAA NIH HHS R21 AA024935NIDDK NIH HHS P30 DK034989NIDDK NIH HHS R01 DK080440NIDDK NIH HHS R01 DK104656NIEHS NIH HHS R01 ES025909
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a common form of cancer with prevalence worldwide. There are many factors that lead to the development and progression of HCC. This study aimed to identify potential new tumor suppressors, examine their function as cell cycle modulators, and investigate their impact on the cyclin family of proteins and cyclin-dependent kinases (CDKs). In this study, the pyruvate dehydrogenase kinase (PDK)4 gene was shown to have potential tumor suppressor characteristics. PDK4 expression was significantly downregulated in human HCC. Pdk4

Indexed as

AnimalsArsenicCarcinoma, HepatocellularCell ProliferationCyclinsDisease ProgressionE2F1 Transcription FactorFlow CytometryHepatocytesLiverLiver NeoplasmsMaleMice, Inbred C57BLProtein KinasesSequence Analysis, RNAArsenicCyclinsE2F1 Transcription FactorProtein Kinasespyruvate dehydrogenase kinase 4

Identifiers

PMID28003426
PMCPMC5325080
OpenAlexW2566718902

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.