Evidence map›Paper›PMID 25404613›Full record

ReviewJournal of molecular cell biology2014

CHK2 kinase in the DNA damage response and beyond.

Laura Zannini, Domenico Delia, Giacomo Buscemi

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 267 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
267citing papers in PubMed, 1 pooled it
8.7field-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

267 citing papers in PubMed, 1 synthesis or guideline pooled it, 441 citations in OpenAlex.

  1. Pooled it
  2. Clinical outcomes of prexasertib monotherapy in recurrentJournal for immunotherapy of cancer · 2020
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207 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

3 authors at 2 institutions in 1 country.

Laura ZanniniDepartment of Experimental Oncology, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42, 20133 Milan, Italy.
Domenico DeliaDepartment of Experimental Oncology, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42, 20133 Milan, Italy giacomo.buscemi@unimi.it domenico.delia@istitutotumori.mi.it.
Giacomo BuscemiDepartment of Biosciences, University of Milan, via Celoria 26, 20133 Milan, Italy giacomo.buscemi@unimi.it domenico.delia@istitutotumori.mi.it.
University of Milan · ITFondazione IRCCS Istituto Nazionale dei Tumori · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The serine/threonine kinase CHK2 is a key component of the DNA damage response. In human cells, following genotoxic stress, CHK2 is activated and phosphorylates >20 proteins to induce the appropriate cellular response, which, depending on the extent of damage, the cell type, and other factors, could be cell cycle checkpoint activation, induction of apoptosis or senescence, DNA repair, or tolerance of the damage. Recently, CHK2 has also been found to have cellular functions independent of the presence of nuclear DNA lesions. In particular, CHK2 participates in several molecular processes involved in DNA structure modification and cell cycle progression. In this review, we discuss the activity of CHK2 in response to DNA damage and in the maintenance of the biological functions in unstressed cells. These activities are also considered in relation to a possible role of CHK2 in tumorigenesis and, as a consequence, as a target of cancer therapy.

Indexed as

Cell Cycle CheckpointsDNA DamageAnimalsCell Transformation, NeoplasticCheckpoint Kinase 2HumansPhosphorylationCheckpoint Kinase 2CHEK2 protein, humanapoptosischeckpointsDNA damagegenomic stability

Identifiers

PMID25404613
PMCPMC4296918
OpenAlexW1484740038

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.