Evidence map›Paper›PMID 24746669›Full record

ArticleDevelopmental cell2014

Cyclin B1/Cdk1 coordinates mitochondrial respiration for cell-cycle G2/M progression.

Zhaoqing Wang, Ming Fan, Demet Candas, Tie-Qiao Zhang, Lili Qin, Angela Eldridge, Sebastian Wachsmann-Hogiu, Kazi M Ahmed, Brett A Chromy, Danupon Nantajit and 6 more

Abstract read
In one paragraph

Article in Developmental cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
214citing papers in PubMed, 1 pooled it
8.5field-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

214 citing papers in PubMed, 1 synthesis or guideline pooled it, 383 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  6. Review
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  9. FTO-mediated mActa pharmaceutica Sinica. B · 2026
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  18. The Effect ofLife (Basel, Switzerland) · 2025
    Article
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  20. Article

154 more citing papers are in PubMed but not listed here.

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

16 authors at 4 institutions in 2 countries.

Zhaoqing WangDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Ming FanDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Demet CandasDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Tie-Qiao ZhangCenter for Biophotonics Science and Technology, University of California, Davis, Sacramento, CA 95817, USA.
Lili QinDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Angela EldridgeDepartment of Pathology and Laboratory Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Sebastian Wachsmann-HogiuCenter for Biophotonics Science and Technology, University of California, Davis, Sacramento, CA 95817, USA.
Kazi M AhmedLife Sciences Division, Department of Cancer and DNA Damage Response, Lawrence Berkeley National Laboratory, University of California, Berkeley, Berkeley, CA 94720, USA.
Brett A ChromyDepartment of Pathology and Laboratory Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Danupon NantajitDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Nadire DuruDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Fuchu HeState Key Laboratory of Proteomics, Beijing Proteomics Research Center, Beijing 102206, China.
Min ChenSignal Transduction Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Toren FinkelCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Lee S WeinsteinSignal Transduction Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Jian Jian LiDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA; NCI-Designated Comprehensive Cancer Center, University of California Davis School of Medicine, Sacramento, CA 95817, USA. Electronic address: jijli@ucdavis.edu.
University of California, Davis · USNational Institutes of Health · USBeijing Proteome Research Center · CNUniversity of California, Berkeley · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura Marcu · 2002 to 2026
$84.9M
Role of the Gnas Gene in Metabolic RegulationZIADK043313 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI WEINSTEIN, LEE · 2009 to 2025
$4.9M
Target MKP-1 for Therapy-Resistant Breast Cancer Stem CellsR01CA152313 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LI, JIAN JIAN · 2011 to 2015
$1.9M
NF-kB-mediated HER-2 overexpression in radioresistant breast cancer stem cells?R01CA133402 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LI, JIAN JIAN · 2009 to 2013
$1.5M
Intramural NIH HHSNCI NIH HHS CA133402NCI NIH HHS CA152313NCI NIH HHS P30 CA093373NCI NIH HHS R01 CA133402NCI NIH HHS R01 CA152313
6 · The paper itself

Abstract

A substantial amount of mitochondrial energy is required for cell-cycle progression. The mechanisms underlying the coordination of the mitochondrial respiration with cell-cycle progression, especially the G2/M transition, remain to be elucidated. Here, we show that a fraction of cyclin B1/Cdk1 proteins localizes to the matrix of mitochondria and phosphorylates a cluster of mitochondrial proteins, including the complex I (CI) subunits in the respiratory chain. Cyclin B1/Cdk1-mediated CI phosphorylation enhances CI activity, whereas deficiency of such phosphorylation in each of the relevant CI subunits results in impairment of CI function. Mitochondria-targeted cyclin B1/Cdk1 increases mitochondrial respiration with enhanced oxygen consumption and ATP generation, which provides cells with efficient bioenergy for G2/M transition and shortens overall cell-cycle time. Thus, cyclin B1/Cdk1-mediated phosphorylation of mitochondrial substrates allows cells to sense and respond to increased energy demand for G2/M transition and, subsequently, to upregulate mitochondrial respiration for successful cell-cycle progression.

Indexed as

AnimalsCDC2 Protein KinaseCell DivisionCyclin B1Cyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesElectron TransportEpithelial CellsG2 PhaseHumansKeratinocytesLiverMCF-7 CellsMiceMitochondriaMitochondrial ProteinsCCNB1 protein, humanCcnb1 protein, mouseCDC2 Protein KinaseCyclin B1Cyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesMitochondrial Proteins

Identifiers

PMID24746669
PMCPMC4156313
OpenAlexW2015807143

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.