Evidence map›Paper›PMID 23708659›Full record

ArticleOncogene2014

RSK promotes G2/M transition through activating phosphorylation of Cdc25A and Cdc25B.

C F Wu, S Liu, Y-C Lee, R Wang, S Sun, F Yin, W G Bornmann, L-Y Yu-Lee, G E Gallick, W Zhang and 2 more

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-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

21 citing papers in PubMed, 31 citations in OpenAlex.

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  18. MicroRNA-211, a direct negative regulator of CDC25B expression, inhibits triple-negative breast cancer cells' growth and migration.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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  20. High expression of Cdc25B and low expression of 14-3-3σ is associated with the development and poor prognosis in urothelial carcinoma of bladder.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    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

12 authors at 4 institutions in 2 countries.

C F WuDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
S LiuThe Key Laboratory for Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, China.
Y-C LeeDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
R WangDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
S Sun1] Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX, USA.
F YinThe Key Laboratory for Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, China.
W G BornmannDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
L-Y Yu-LeeDepartment of Medicine, Baylor College of Medicine, Houston, TX, USA.
G E Gallick1] The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX, USA [2] Department of Genitourinary Medical Oncology Research, David H. Koch Center for Applied Research of Genitourinary Cancers, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
W ZhangThe Key Laboratory for Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, China.
S-H Lin1] Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX, USA.
J Kuang1] Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · USBeijing Normal University · CNUniversity of Houston · USBaylor College of Medicine · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting Tumor Microenvironment-Induced Therapy Resistance in Prostate Cancer Bone MetastasisP50CA140388 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGOTHETIS, CHRISTOPHER J., THOMPSON, TIMOTHY CHARLES · 2009 to 2022
$23.4M
NCI NIH HHS CA016672NCI NIH HHS CA140388NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA140388
6 · The paper itself

Abstract

Activation of the mitogen-activated protein kinase (MAPK) cascade in mammalian cell lines positively regulates the G2/M transition. The molecular mechanism underlying this biological phenomenon remains poorly understood. Ribosomal S6 kinase (RSK) is a key downstream element of the MAPK cascade. Our previous studies established roles of RSK2 in Cdc25C activation during progesterone-induced meiotic maturation of Xenopus oocytes. In this study we demonstrate that both recombinant RSK and endogenous RSK in Xenopus egg extracts phosphorylate all three isoforms of human Cdc25 at a conserved motif near the catalytic domain. In human HEK293 and PC-3mm2 cell lines, RSK preferentially phosphorylates Cdc25A and Cdc25B in mitotic cells. Phosphorylation of the RSK sites in these Cdc25 isoforms increases their M-phase-inducing activities. Inhibition of RSK-mediated phosphorylation of Cdc25 inhibits G2/M transition. Moreover, RSK is likely to be more active in mitotic cells than in interphase cells, as evidenced by the phosphorylation status of T359/S363 in RSK. Together, these findings indicate that RSK promotes G2/M transition in mammalian cells through activating phosphorylation of Cdc25A and Cdc25B.

Indexed as

G2 Phase Cell Cycle CheckpointsAmino Acid SequenceAnimalscdc25 PhosphatasesHEK293 CellsHumansMolecular Sequence DataOocytesPhosphorylationRibosomal Protein S6 Kinases, 90-kDaXenopusCDC25A protein, humanCDC25B protein, humancdc25 Phosphatasesribosomal protein S6 kinase, 90kDa, polypeptide 3Ribosomal Protein S6 Kinases, 90-kDa

Identifiers

PMID23708659
PMCPMC4026278
OpenAlexW2011913495

What OpenQuestion holds

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Registered trials

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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.