Evidence map›Paper›PMID 34671219›Full record

ReviewInternational journal of biological sciences2021

Post-Translational Modifications of PCNA in Control of DNA Synthesis and DNA Damage Tolerance-the Implications in Carcinogenesis.

Siyi Zhang, Tingting Zhou, Zhuo Wang, Fei Yi, Chunlu Li, Wendong Guo, Hongde Xu, Hongyan Cui, Xiang Dong, Jingwei Liu and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

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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

12 authors at 3 institutions in 2 countries.

Siyi ZhangInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Tingting ZhouInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Zhuo WangInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Fei YiInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Chunlu LiInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Wendong GuoInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Hongde XuInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Hongyan CuiInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Xiang DongInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Jingwei LiuInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Xiaoyu SongInstitute of Health Sciences, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
Liu CaoCollege of Basic Medical Science, Key Laboratory of Cell Biology of Ministry of Public Health, Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, Shenyang, Liaoning Province, 110122, PR China.
China Medical University · CNMinistry of Education · KNShenyang Center for Disease Control and Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The faithful DNA replication is a critical event for cell survival and inheritance. However, exogenous or endogenous sources of damage challenge the accurate synthesis of DNA, which causes DNA lesions. The DNA lesions are obstacles for replication fork progression. However, the prolonged replication fork stalling leads to replication fork collapse, which may cause DNA double-strand breaks (DSB). In order to maintain genomic stability, eukaryotic cells evolve translesion synthesis (TLS) and template switching (TS) to resolve the replication stalling. Proliferating cell nuclear antigen (PCNA) trimer acts as a slide clamp and encircles DNA to orchestrate DNA synthesis and DNA damage tolerance (DDT). The post-translational modifications (PTMs) of PCNA regulate these functions to ensure the appropriate initiation and termination of replication and DDT. The aberrant regulation of PCNA PTMs will result in DSB, which causes mutagenesis and poor response to chemotherapy. Here, we review the roles of the PCNA PTMs in DNA duplication and DDT. We propose that clarifying the regulation of PCNA PTMs may provide insights into understanding the development of cancers.

Indexed as

CarcinogenesisDNA DamageDNA ReplicationProtein Processing, Post-TranslationalHumansProliferating Cell Nuclear AntigenPCNA protein, humanProliferating Cell Nuclear AntigenacetylationDDTISGylationNEDDylationphosphorylationreplicationSUMOylationubiquitination

Identifiers

PMID34671219
PMCPMC8495385
OpenAlexW3207499161

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.