Evidence map›Paper›PMID 33967572›Full record

ReviewSeminars in cell & developmental biology2021

Making Choices: DNA Replication Fork Recovery Mechanisms.

Christine M Kondratick, M Todd Washington, Maria Spies

Open access · bronzeAbstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
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  6. Review
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  12. bioRxiv : the preprint server for biology · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Helicase HELQ: Molecular Characters Fit for DSB Repair Function.International journal of molecular sciences · 2024
    Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Christine M KondratickDepartment of Biochemistry, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242.
M Todd WashingtonDepartment of Biochemistry, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242.
Maria SpiesDepartment of Biochemistry, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242.
University of Iowa · US

Funding

Mechanisms of Damaged DNA Replication in EukaryotesR01GM081433 · NIGMS · UNIVERSITY OF IOWA · PI WASHINGTON, M. TODD · 2008 to 2021
$4.2M
Assembly and Dynamics of Molecular Machines in Genome MaintenanceR35GM131704 · NIGMS · UNIVERSITY OF IOWA · PI Maria Spies · 2019 to 2026
$3.9M
The Role of Human RAD52 Protein in Genome StabilityR01CA232425 · NCI · UNIVERSITY OF IOWA · PI Maria Spies · 2019 to 2026
$3.1M
NCI NIH HHS R01 CA232425NIGMS NIH HHS R01 GM081433NIGMS NIH HHS R35 GM131704
6 · The paper itself

Abstract

DNA replication is laden with obstacles that slow, stall, collapse, and break DNA replication forks. At each obstacle, there is a decision to be made whether to bypass the lesion, repair or restart the damaged fork, or to protect stalled forks from further demise. Each "decision" draws upon multitude of proteins participating in various mechanisms that allow repair and restart of replication forks. Specific functions for many of these proteins have been described and an understanding of how they come together in supporting replication forks is starting to emerge. Many questions, however, remain regarding selection of the mechanisms that enable faithful genome duplication and how "normal" intermediates in these mechanisms are sometimes funneled into "rogue" processes that destabilize the genome and lead to cancer, cell death, and emergence of chemotherapeutic resistance. In this review we will discuss molecular mechanisms of DNA damage bypass and replication fork protection and repair. We will specifically focus on the key players that define which mechanism is employed including: PCNA and its control by posttranslational modifications, translesion synthesis DNA polymerases, molecular motors that catalyze reversal of stalled replication forks, proteins that antagonize fork reversal and protect reversed forks from nucleolytic degradation, and the machinery of homologous recombination that helps to reestablish broken forks. We will also discuss risks to genome integrity inherent in each of these mechanisms.

Indexed as

DNA DamageDNA ReplicationHumansBRCA2DNA replicationgenome stabilityHLTFPCNARAD51RAD52replication fork protectionreplication fork reversalRPASHPRHSMARCAL1template switchingtranslesion synthesistranslesion synthesis DNA polymerasesZRANB3

Identifiers

PMID33967572
PMCPMC8098667
OpenAlexW3094475318

What OpenQuestion holds

Textmetadata
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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.