Evidence map›Paper›PMID 28739856›Full record

ArticleMolecular and cellular biology2017

CKS Proteins Promote Checkpoint Recovery by Stimulating Phosphorylation of Treslin.

Ruiling Mu, John Tat, Robert Zamudio, Yaoyang Zhang, John R Yates, Akiko Kumagai, William G Dunphy, Steven I Reed

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular and cellular biology, 2017. 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
0.2field-weighted citation impact, top 44% 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, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. 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 2 institutions in 1 country.

Ruiling MuDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.
John TatDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.
Robert ZamudioDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.
Yaoyang ZhangDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.
John R YatesDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.
Akiko KumagaiDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, California, USA.
William G DunphyDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, California, USA.
Steven I ReedDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA sreed@scripps.edu.
Scripps Research Institute · USCalifornia Institute of Technology · US

Funding

Scripps Translational Science InstituteUL1TR001114 · NCATS · SCRIPPS RESEARCH INSTITUTE, THE · PI TOPOL, ERIC JEFFREY · 2013 to 2017
$24.0M
TrainingP41GM103533 · NIGMS · UNIVERSITY OF WASHINGTON · PI MACCOSS, MICHAEL · 2012 to 2021
$20.7M
The role of Cyclin E in growth control and tumorogenesisR01CA078343 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI REED, STEVEN I · 1998 to 2019
$8.1M
Role of ATR in Cell Cycle CheckpointsR01GM070891 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI DUNPHY, WILLIAM G · 2004 to 2018
$5.7M
CKS PROTEINS IN CELL CYCLE CONTROL AND TUMOROGENESISR01CA074224 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI REED, STEVEN I · 1997 to 2012
$4.6M
ENZYMOLOGY OF MITOSIS PROMOTING FACTOR (MPF)R01GM043974 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI DUNPHY, WILLIAM G · 1990 to 2022
$4.0M
Enzymology of Mitosis Promoting Factor (MPF)R37GM043974 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI DUNPHY, WILLIAM G · 2002 to 2011
$4.0M
The role of Cyclin E in growth control and tumorogenesisR56CA078343 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI REED, STEVEN I · 2008 to 2008
$348k
NCATS NIH HHS UL1 TR001114NCI NIH HHS R01 CA074224NCI NIH HHS R01 CA078343NCI NIH HHS R56 CA078343NIGMS NIH HHS P41 GM103533NIGMS NIH HHS R01 GM043974NIGMS NIH HHS R01 GM070891NIGMS NIH HHS R37 GM043974
6 · The paper itself

Abstract

CKS proteins are small (9-kDa) polypeptides that bind to a subset of the cyclin-dependent kinases. The two paralogs expressed in mammals, Cks1 and Cks2, share an overlapping function that is essential for early development. However, both proteins are frequently overexpressed in human malignancy. It has been shown that CKS protein overexpression overrides the replication stress checkpoint, promoting continued origin firing. This finding has led to the proposal that CKS protein-dependent checkpoint override allows premalignant cells to evade oncogene stress barriers, providing a causal link to oncogenesis. Here, we provide mechanistic insight into how overexpression of CKS proteins promotes override of the replication stress checkpoint. We show that CKS proteins greatly enhance the ability of Cdk2 to phosphorylate the key replication initiation protein treslin

Indexed as

Carrier ProteinsCDC2-CDC28 KinasesCell Cycle CheckpointsCell Cycle ProteinsDNA DamageDNA ReplicationHumansPhosphorylationCarrier ProteinsCDC2-CDC28 KinasesCell Cycle ProteinsCKS1B protein, humanCKS2 protein, humanTICRR protein, humancheckpoint recoveryCKS proteinreplication stress checkpointtreslintreslin phosphorylation

Identifiers

PMID28739856
PMCPMC5615187
OpenAlexW2737027255

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.