Evidence map›Paper›PMID 31167143›Full record

ArticleCell reports2019

Phosphorylation of FANCD2 Inhibits the FANCD2/FANCI Complex and Suppresses the Fanconi Anemia Pathway in the Absence of DNA Damage.

David Lopez-Martinez, Marian Kupculak, Di Yang, Yasunaga Yoshikawa, Chih-Chao Liang, Ronghu Wu, Steven P Gygi, Martin A Cohn

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  12. Screening and identification of novel candidate biomarkers of focal cortical dysplasia type II via bioinformatics analysis.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2022
    Article
  13. Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021
    Review
  14. Review
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  17. Oncogenic HPV promotes the expression of the long noncoding RNA lnc-FANCI-2 through E7 and YY1.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

8 authors at 2 institutions in 2 countries.

David Lopez-MartinezDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.
Marian KupculakDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.
Di YangDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.
Yasunaga YoshikawaDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.
Chih-Chao LiangDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.
Ronghu WuDepartment of Cell Biology, Harvard Medical School, Boston, MA 01125, USA.
Steven P GygiDepartment of Cell Biology, Harvard Medical School, Boston, MA 01125, USA.
Martin A CohnDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, UK. Electronic address: martin.cohn@bioch.ox.ac.uk.
University of Oxford · GBHarvard University · US

Funding

New Sample Multiplexing Technologies to Identify Chemical Probes and Illuminate Ubiquitin BiologyR01GM067945 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI GYGI, STEVEN P · 2003 to 2024
$10.5M
Cancer Research UKMedical Research Council MR/N021002/1NIGMS NIH HHS R01 GM067945Wellcome TrustWellcome Trust 210640/Z/18/Z
6 · The paper itself

Abstract

Interstrand crosslinks (ICLs) of the DNA helix are a deleterious form of DNA damage. ICLs can be repaired by the Fanconi anemia pathway. At the center of the pathway is the FANCD2/FANCI complex, recruitment of which to DNA is a critical step for repair. After recruitment, monoubiquitination of both FANCD2 and FANCI leads to their retention on chromatin, ensuring subsequent repair. However, regulation of recruitment is poorly understood. Here, we report a cluster of phosphosites on FANCD2 whose phosphorylation by CK2 inhibits both FANCD2 recruitment to ICLs and its monoubiquitination in vitro and in vivo. We have found that phosphorylated FANCD2 possesses reduced DNA binding activity, explaining the previous observations. Thus, we describe a regulatory mechanism operating as a molecular switch, where in the absence of DNA damage, the FANCD2/FANCI complex is prevented from loading onto DNA, effectively suppressing the FA pathway.

Indexed as

Amino Acid SequenceAnimalsCasein Kinase IICRISPR-Cas SystemsDNADNA DamageDNA RepairFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsHeLa CellsHumansPhosphorylationProtein BindingProtein Structure, QuaternaryRNA, Guide, CRISPR-Cas SystemsCasein Kinase IIDNAFANCD2 protein, humanFANCI protein, humanFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsRNA, Guide, CRISPR-Cas Systemscasein kinase 2CK2DNA repairFANCD2/FANCIFanconi anemiagenome stabilityICL repairinterstrand crosslink repairkinasephosphorylation

Identifiers

PMID31167143
PMCPMC6581795
OpenAlexW2948086251

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.