Evidence map›Paper›PMID 35017203›Full record

ArticleLife science alliance2022

Chl1 helicase controls replication fork progression by regulating dNTP pools.

Amandine Batté, Sophie C van der Horst, Mireille Tittel-Elmer, Su Ming Sun, Sushma Sharma, Jolanda van Leeuwen, Andrei Chabes, Haico van Attikum

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 54% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

8 authors at 3 institutions in 3 countries.

Amandine BattéDepartment of Human Genetics, Leiden University Medical Center, Leiden, Netherlands.ORCID 0000-0002-6918-5782
Sophie C van der HorstDepartment of Human Genetics, Leiden University Medical Center, Leiden, Netherlands.ORCID 0000-0002-9347-7240
Mireille Tittel-ElmerDepartment of Human Genetics, Leiden University Medical Center, Leiden, Netherlands.
Su Ming SunDepartment of Human Genetics, Leiden University Medical Center, Leiden, Netherlands.
Sushma SharmaDepartment of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.ORCID 0000-0003-2713-5813
Jolanda van LeeuwenCenter for Integrative Genomics, Université de Lausanne, Lausanne-Dorigny, Switzerland.ORCID 0000-0003-3991-518X
Andrei ChabesDepartment of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.
Haico van AttikumDepartment of Human Genetics, Leiden University Medical Center, Leiden, Netherlands h.van.attikum@lumc.nl.ORCID 0000-0001-8590-0240
Leiden University Medical Center · NLUmeå University · SEUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eukaryotic cells have evolved a replication stress response that helps to overcome stalled/collapsed replication forks and ensure proper DNA replication. The replication checkpoint protein Mrc1 plays important roles in these processes, although its functional interactions are not fully understood. Here, we show that

Indexed as

Cell Cycle ProteinsCells, CulturedChromosomal Proteins, Non-HistoneDEAD-box RNA HelicasesDeoxyribonucleotidesDNA HelicasesDNA ReplicationHumansSaccharomyces cerevisiae ProteinsCell Cycle ProteinsCHL1 protein, S cerevisiaeChromosomal Proteins, Non-HistoneDDX11 protein, humanDEAD-box RNA HelicasesDeoxyribonucleotidesDNA HelicasesMRC1 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID35017203
PMCPMC8761496
OpenAlexW4206543179

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.