Evidence map›Paper›PMID 30808711›Full record

ArticleThe Journal of biological chemistry2019

Nucleotide excision repair capacity increases during differentiation of human embryonic carcinoma cells into neurons and muscle cells.

Wentao Li, Wenjie Liu, Ayano Kakoki, Rujin Wang, Ogun Adebali, Yuchao Jiang, Aziz Sancar

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  8. Mitotic chromatin marking governs asymmetric segregation of DNA damage.bioRxiv : the preprint server for biology · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. CSB-independent, XPC-dependent transcription-coupled repair inProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. Review
  15. Epigenetic Regulation of Nucleotide Excision Repair.Frontiers in cell and developmental biology · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. 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

7 authors at 2 institutions in 3 countries.

Wentao LiFrom the Department of Biochemistry and Biophysics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599.
Wenjie LiuFrom the Department of Biochemistry and Biophysics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599; School of Pharmaceutical Sciences, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, Xiamen, Fujian 361102 China.
Ayano KakokiFrom the Department of Biochemistry and Biophysics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599.
Rujin WangDepartment of Biostatistics, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599.
Ogun AdebaliMolecular Biology, Genetics and Bioengineering Program, Faculty of Engineering and Natural Sciences, Sabanci University, Istanbul 34956 Turkey.
Yuchao JiangDepartment of Biostatistics, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599; Department of Genetics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599.
Aziz SancarFrom the Department of Biochemistry and Biophysics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599. Electronic address: aziz_sancar@med.unc.edu.
University of North Carolina at Chapel Hill · USSabancı Üniversitesi · TR

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A. Troester · 2001 to 2026
$36.3M
Statistical Methods for Cancer Clinical TrialsP01CA142538 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAVIDIAN, MARIE, KOSOROK, MICHAEL R · 2010 to 2019
$21.3M
Molecular Mechanism of Mammalian DNA Excision Repair, DNA Damage Checkpoints and the Circadian ClockR35GM118102 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI AZIZ SANCAR · 2016 to 2026
$10.6M
Single Nucleotide Resolution Map of Formation and Repair of Bulky Adducts in the Human GenomeR01ES027255 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SANCAR, AZIZ · 2016 to 2020
$2.3M
NCI NIH HHS P01 CA142538NIEHS NIH HHS P30 ES010126NIEHS NIH HHS R01 ES027255NIGMS NIH HHS R35 GM118102
6 · The paper itself

Abstract

Embryonic stem cells can self-renew and differentiate, holding great promise for regenerative medicine. They also employ multiple mechanisms to preserve the integrity of their genomes. Nucleotide excision repair, a versatile repair mechanism, removes bulky DNA adducts from the genome. However, the dynamics of the capacity of nucleotide excision repair during stem cell differentiation remain unclear. Here, using immunoslot blot assay, we measured repair rates of UV-induced DNA damage during differentiation of human embryonic carcinoma (NTERA-2) cells into neurons and muscle cells. Our results revealed that the capacity of nucleotide excision repair increases as cell differentiation progresses. We also found that inhibition of the apoptotic signaling pathway has no effect on nucleotide excision repair capacity. Furthermore, RNA-Seq-based transcriptomic analysis indicated that expression levels of four core repair factors, xeroderma pigmentosum (XP) complementation group A (XPA), XPC, XPG, and XPF-ERCC1, are progressively up-regulated during differentiation, but not those of replication protein A (RPA) and transcription factor IIH (TFIIH). Together, our findings reveal that increase of nucleotide excision repair capacity accompanies cell differentiation, supported by the up-regulated transcription of genes encoding DNA repair enzymes during differentiation of two distinct cell lineages.

Indexed as

Cell DifferentiationDNA RepairCell Line, TumorDNA-Binding ProteinsDNA Excision Repair Protein ERCC-5Embryonal Carcinoma Stem CellsEndonucleasesHumansMuscle CellsNeoplasm ProteinsNeuronsNuclear ProteinsReplication Protein ATranscription FactorsTranscription Factor TFIIHXeroderma Pigmentosum Group A ProteinDNA-Binding ProteinsDNA Excision Repair Protein ERCC-5EndonucleasesERCC1 protein, humanNeoplasm ProteinsNuclear ProteinsReplication Protein ARPA1 protein, humanTranscription FactorsTranscription Factor TFIIHXeroderma Pigmentosum Group A Proteinxeroderma pigmentosum group F proteinXPA protein, humanXPC protein, humanbone morphogenetic protein-2 (BMP-2)cancer stem cellscell differentiationdifferentiationgenome stabilitymuscle cellneuronNT2 cellnucleotide excision repairretinoic acid (RA)stem celltranscriptomicsvascular smooth muscle cells

Identifiers

PMID30808711
PMCPMC6463700
OpenAlexW2917027509

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.