Evidence map›Paper›PMID 35976701›Full record

ArticleMolecular biology of the cell2022

Revisiting the multisite phosphorylation that produces the M-phase supershift of key mitotic regulators.

Tan Tan, Chuanfen Wu, Boye Liu, Bih-Fang Pan, David H Hawke, Zehao Su, Shuaishuai Liu, Wei Zhang, Ruoning Wang, Sue-Hwa Lin and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. 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

11 authors at 3 institutions in 3 countries.

Tan TanDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Chuanfen WuDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Boye LiuKey Laboratory for Biodiversity and Ecological Engineering of Ministry of Education.
Bih-Fang PanDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
David H HawkeDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Zehao SuKey Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing 100875, China.
Shuaishuai LiuKey Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing 100875, China.
Wei ZhangKey Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing 100875, China.
Ruoning WangDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Sue-Hwa LinDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Jian KuangDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
The University of Texas MD Anderson Cancer Center · USBeijing Normal University · CNMinistry of Education · IR

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 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 THOMPSON, TIMOTHY CHARLES · 2009 to 2022
$23.4M
Metabolic programming in TH17 cell differentiationR01AI114581 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI WANG, RUONING · 2015 to 2025
$3.6M
Endothelial-to-osteoblast transition in prostate cancer bone metastasisR01CA174798 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LIN, SUE-HWA · 2013 to 2023
$3.0M
Modulation of asparagine bioavailability and stress response signaling to enhance T cell robustness and maximize immunotherapyR01CA247941 · NCI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI WANG, RUONING · 2021 to 2025
$2.4M
Decipher and target GABA metabolism and GABA receptor-mediated signaling in autoimmune diseasesR01AI175004 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI Ruoning Wang · 2023 to 2026
$2.0M
Orbitrap Elite High-Resolution Mass Spectrometer for Proteomics and MetabolomicsS10OD012304 · OD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HAWKE, DAVID H · 2013 to 2013
$877k
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA140388NCI NIH HHS R01 CA174798NCI NIH HHS R01 CA247941NIAID NIH HHS R01 AI114581NIAID NIH HHS R01 AI175004NIH HHS S10 OD012304
6 · The paper itself

Abstract

The term M-phase supershift denotes the phosphorylation-dependent substantial increase in the apparent molecular weight of numerous proteins of varied biological functions during M-phase induction. Although the M-phase supershift of multiple key mitotic regulators has been attributed to the multisite phosphorylation catalyzed by the Cdk1/cyclin B/Cks complex, this view is challenged by multiple lines of paradoxical observations. To solve this problem, we reconstituted the M-phase supershift of Xenopus Cdc25C, Myt1, Wee1A, APC3, and Greatwall in Xenopus egg extracts and characterized the supershift-producing phosphorylations. Our results demonstrate that their M-phase supershifts are each due to simultaneous phosphorylation of a considerable portion of S/T/Y residues in a long intrinsically disordered region that is enriched in both S/T residues and S/TP motifs. Although the major mitotic kinases in Xenopus egg extracts, Cdk1, MAPK, Plx1, and RSK2, are able to phosphorylate the five mitotic regulators, they are neither sufficient nor required to produce the M-phase supershift. Accordingly, inhibition of the four major mitotic kinase activities in Xenopus oocytes did not inhibit the M-phase supershift in okadaic acid-induced oocyte maturation. These findings indicate that the M-phase supershift is produced by a previously unrecognized category of mitotic phosphorylation that likely plays important roles in M-phase induction.

Indexed as

Cell Cycle ProteinsXenopus ProteinsAnimalsCDC2 Protein KinaseCyclin BMitosisOkadaic AcidOocytesPhosphorylationXenopus laevisCDC2 Protein KinaseCell Cycle ProteinsCyclin BOkadaic AcidXenopus Proteins

Identifiers

PMID35976701
PMCPMC9635296
OpenAlexW4292104453

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.