Evidence map›Paper›PMID 29886395›Full record

ReviewRedox biology2018

PARP1 promoter links cell cycle progression with adaptation to oxidative environment.

Julita Pietrzak, Corinne M Spickett, Tomasz Płoszaj, László Virág, Agnieszka Robaszkiewicz

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-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

30 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  16. Review
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  18. Food science & nutrition · 2022
    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

5 authors at 4 institutions in 3 countries.

Julita PietrzakDepartment of General Biophysics, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.
Corinne M SpickettSchool of Life & Health Sciences, Aston University, Aston Triangle, Birmingham B4 7ET, UK.
Tomasz PłoszajDepartment of Molecular Biology, Medical University of Lodz, Narutowicza 60, 90-136 Lodz, Poland.
László VirágDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary; MTA-DE Cell Biology and Signaling Research Group, Debrecen, Hungary.
Agnieszka RobaszkiewiczDepartment of General Biophysics, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland. Electronic address: agnieszka.robaszkiewicz@biol.uni.lodz.pl.
University of Łódź · PLAston University · GBMedical University of Lodz · PLUniversity of Debrecen · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although electrophiles are considered as detrimental to cells, accumulating recent evidence indicates that proliferating non-cancerous and particularly cancerous cells utilize these agents for pro-survival and cell cycle promoting signaling. Hence, the redox shift to mild oxidant release must be balanced by multiple defense mechanisms. Our latest findings demonstrate that cell cycle progression, which dictates oxidant level in stress-free conditions, determines PARP1 transcription. Growth modulating factors regulate CDK4/6-RBs-E2Fs axis. In cells arrested in G1 and G0, RB1-E2F1 and RBL2-E2F4 dimers recruit chromatin remodelers such as HDAC1, SWI/SNF and PRC2 to condense chromatin and turn off transcription. Release of retinoblastoma-based repressive complexes from E2F-dependent gene promoters in response to cell transition to S phase enables transcription of PARP1. This enzyme contributes to repair of oxidative DNA damage by supporting several strand break repair pathways and nucleotide or base excision repair pathways, as well as acting as a co-activator of transcription factors such as NRF2 and HIF1a, which control expression of antioxidant enzymes involved in removal of electrophiles and secondary metabolites. Furthermore, PARP1 is indispensible for transcription of the pro-survival kinases MAP2K6, ERK1/2 and AKT1, and for maintaining MAPK activity by suppressing transcription of the MAPK inhibitor, MPK1. In summary, cell cycle controlled PARP1 transcription helps cells to adapt to a pro-oxidant redox shift.

Indexed as

Cell CycleOxidative StressPromoter Regions, GeneticTranscriptional ActivationAnimalsCell ProliferationDNA RepairHumansPoly (ADP-Ribose) Polymerase-1Signal TransductionPoly (ADP-Ribose) Polymerase-1Cell proliferationDNA repairGene transcriptionPoly-ADP-ribose polymerase 1 (PARP1)Redox homeostasisSignaling

Identifiers

PMID29886395
PMCPMC5991907
OpenAlexW2806607013

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.