Evidence map›Paper›PMID 31597704›Full record

ArticleThe Journal of biological chemistry2019

5-Formylcytosine-induced DNA-peptide cross-links reduce transcription efficiency, but do not cause transcription errors in human cells.

Shaofei Ji, Daeyoon Park, Konstantin Kropachev, Marina Kolbanovskiy, Iwen Fu, Suse Broyde, Maram Essawy, Nicholas E Geacintov, Natalia Y Tretyakova

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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. DNA polymerases η and κ bypass NThe Journal of biological chemistry · 2021
    Article
  9. Comparative Nucleosomal Reactivity of 5-Formyl-Uridine and 5-Formyl-Cytidine.Chemistry (Weinheim an der Bergstrasse, Germany) · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Enzymatic bypass of an NThe Journal of biological chemistry
    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

9 authors at 2 institutions in 1 country.

Shaofei JiDepartment of Chemistry, University of Minnesota, Minneapolis, Minnesota 55455.
Daeyoon ParkDepartment of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, Minnesota 55455.
Konstantin KropachevDepartment of Chemistry, New York University, New York, New York 10003.
Marina KolbanovskiyDepartment of Chemistry, New York University, New York, New York 10003.
Iwen FuDepartment of Biology, New York University, New York, New York 10003.
Suse BroydeDepartment of Biology, New York University, New York, New York 10003.
Maram EssawyDepartment of Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455.
Nicholas E GeacintovDepartment of Chemistry, New York University, New York, New York 10003.
Natalia Y TretyakovaDepartment of Medicinal Chemistry, University of Minnesota, Minneapolis, Minnesota 55455; Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota 55455. Electronic address: trety001@umn.edu.
New York University · USUniversity of Minnesota · US

Funding

DNA Protein Cross-Links:Cellular Effects and Repair MechanismsR01ES023350 · NIEHS · UNIVERSITY OF MINNESOTA · PI CAMPBELL, COLIN R, TRETYAKOVA, NATALIA Y · 2014 to 2023
$5.0M
Environmental DNA Lesions and Mutagenesis: Molecular Mechanisms of Lesion Recognition for Repair and Polymerase BypassR01ES025987 · NIEHS · NEW YORK UNIVERSITY · PI BROYDE, SUSE · 2016 to 2025
$3.6M
Recognition of Environmental Carcinogen-DNA lesions by NER ProteinsR01ES024050 · NIEHS · NEW YORK UNIVERSITY · PI GEACINTOV, NICHOLAS E · 2014 to 2018
$1.8M
NIEHS NIH HHS R01 ES023350NIEHS NIH HHS R01 ES024050NIEHS NIH HHS R01 ES025987
6 · The paper itself

Abstract

5-Formylcytosine (5fC) is an endogenous epigenetic DNA mark introduced via enzymatic oxidation of 5-methyl-dC in DNA. We and others recently reported that 5fC can form reversible DNA-protein conjugates with histone proteins, likely contributing to regulation of nucleosomal organization and gene expression. The protein component of DNA-protein cross-links can be proteolytically degraded, resulting in smaller DNA-peptide cross-links. Unlike full-size DNA-protein cross-links that completely block replication and transcription, DNA-peptide cross-links can be bypassed by DNA and RNA polymerases and can potentially be repaired via the nucleotide excision repair (NER) pathway. In the present work, we constructed plasmid molecules containing reductively stabilized, site-specific 5fC-polypeptide lesions and employed a quantitative MS-based assay to assess their effects on transcription in cells. Our results revealed that the presence of DNA-peptide cross-link significantly inhibits transcription in human HEK293T cells but does not induce transcription errors. Furthermore, transcription efficiency was similar in WT and NER-deficient human cell lines, suggesting that the 5fC-polypeptide lesion is a weak substrate for NER. This finding was confirmed by

Indexed as

Transcription, GeneticCell LineCross-Linking ReagentsCytosineDNADNA Breaks, Double-StrandedDNA RepairDNA ReplicationHEK293 CellsHeLa CellsHumansPeptides5-formylcytosineCross-Linking ReagentsCytosineDNAPeptides5-formylcytosinebulky DNA lesionDNA damageDNA–peptide cross-linkDNA transcriptionepigenetic markepigeneticsgene regulationhuman cellsnucleotide excision repairprotein cross-linkingRNA polymerase IItranscription

Identifiers

PMID31597704
PMCPMC6885644
OpenAlexW2979591665

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.