Evidence map›Paper›PMID 34096775›Full record

ArticleMolecular and cellular biology2021

Cyclin-Dependent Kinase-Mediated Phosphorylation of FANCD2 Promotes Mitotic Fidelity.

Juan A Cantres-Velez, Justin L Blaize, David A Vierra, Rebecca A Boisvert, Jada L Garzon, Benjamin Piraino, Winnie Tan, Andrew J Deans, Niall G Howlett

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021
    Review
  6. 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 3 institutions in 2 countries.

Juan A Cantres-VelezDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
Justin L BlaizeDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
David A VierraDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
Rebecca A BoisvertDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
Jada L GarzonDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.
Benjamin PirainoDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
Winnie TanGenome Stability Unit, St. Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia.
Andrew J DeansGenome Stability Unit, St. Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia.
Niall G HowlettDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
University of Rhode Island · USSt Vincents Institute of Medical Research · AUHarvard University · US

Funding

Training CoreP20GM103430 · NIGMS · UNIVERSITY OF RHODE ISLAND · PI Christopher Lee Hemme · 2012 to 2026
$63.6M
Chromatin State Alterations in Fanconi Anemia Hematologic Disease and Bone Marrow FailureR01HL149907 · NHLBI · UNIVERSITY OF RHODE ISLAND · PI HOWLETT, NIALL GEORGE · 2020 to 2023
$1.2M
NHLBI NIH HHS R01 HL149907NIGMS NIH HHS P20 GM103430
6 · The paper itself

Abstract

Fanconi anemia (FA) is a rare genetic disease characterized by increased risk for bone marrow failure and cancer. The FA proteins function together to repair damaged DNA. A central step in the activation of the FA pathway is the monoubiquitination of the FANCD2 and FANCI proteins, which occurs upon exposure to DNA-damaging agents and during the S phase of the cell cycle. The regulatory mechanisms governing S-phase monoubiquitination, in particular, are poorly understood. In this study, we have identified a cyclin-dependent kinase (CDK) regulatory phosphosite (S592) proximal to the site of FANCD2 monoubiquitination. FANCD2 S592 phosphorylation was detected by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and by immunoblotting with an S592 phospho-specific antibody. Mutation of S592 leads to abrogated monoubiquitination of FANCD2 during the S phase. Furthermore, FA-D2 (

Indexed as

Cell CycleCyclin-Dependent KinasesFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsHumansPhosphorylationTandem Mass SpectrometryUbiquitinationCyclin-Dependent KinasesFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsCDK phosphorylationcell cyclechromosome stabilityFANCD2Fanconi anemiaubiquitinubiquitination

Identifiers

PMID34096775
PMCPMC8300791
OpenAlexW3171501889

What Socratic 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 Socratic graph.