Evidence map›Paper›PMID 31366665›Full record

ArticleThe Journal of cell biology2019

Basal CHK1 activity safeguards its stability to maintain intrinsic S-phase checkpoint functions.

Jone Michelena, Marco Gatti, Federico Teloni, Ralph Imhof, Matthias Altmeyer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 40 citations in OpenAlex.

  1. Replication stress links Geminin depletion to centrosome amplification.bioRxiv : the preprint server for biology · 2026
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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

5 authors at 1 institution in 1 country.

Jone MichelenaDepartment of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.
Marco GattiDepartment of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.
Federico TeloniDepartment of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-0953-8010
Ralph ImhofDepartment of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.
Matthias AltmeyerDepartment of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland matthias.altmeyer@uzh.ch.ORCID 0000-0003-3780-1170
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA replication machinery frequently encounters impediments that slow replication fork progression and threaten timely and error-free replication. The CHK1 protein kinase is essential to deal with replication stress (RS) and ensure genome integrity and cell survival, yet how basal levels and activity of CHK1 are maintained under physiological, unstressed conditions is not well understood. Here, we reveal that CHK1 stability is controlled by its steady-state activity during unchallenged cell proliferation. This autoactivatory mechanism, which depends on ATR and its coactivator ETAA1 and is tightly associated with CHK1 autophosphorylation at S296, counters CHK1 ubiquitylation and proteasomal degradation, thereby preventing attenuation of S-phase checkpoint functions and a compromised capacity to respond to RS. Based on these findings, we propose that steady-state CHK1 activity safeguards its stability to maintain intrinsic checkpoint functions and ensure genome integrity and cell survival.

Indexed as

Genomic InstabilityProteolysisS Phase Cell Cycle CheckpointsUbiquitinationAntigens, SurfaceAtaxia Telangiectasia Mutated ProteinsCell SurvivalCheckpoint Kinase 1Enzyme StabilityHeLa CellsHumansAntigens, SurfaceAtaxia Telangiectasia Mutated ProteinsATR protein, humanCheckpoint Kinase 1CHEK1 protein, humanETAA1 protein, human

Identifiers

PMID31366665
PMCPMC6719454
OpenAlexW2966373256

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.