FANCM regulates DNA chain elongation and is stabilized by S-phase checkpoint signalling

Publikationstyp:
Zeitschriftenaufsatz
Metadaten:
Autoren
  • Sarah Luke-Glaser
  • Brian Luke
  • Simona Grossi
  • Angelos Constantinou
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000274604600010&DestLinkType=FullRecord&DestApp=WOS_CPL
DOI
10.1038/emboj.2009.371
eISSN
1460-2075
Externe Identifier
  • Clarivate Analytics Document Solution ID: 556PX
  • PubMed Identifier: 20010692
ISSN
0261-4189
Ausgabe der Veröffentlichung
4
Zeitschrift
EMBO JOURNAL
Schlüsselwörter
  • DNA replication
  • FANCM
  • Fanconi anemia
  • fork regression
Paginierung
795 - 805
Datum der Veröffentlichung
2010
Status
Published
Titel
FANCM regulates DNA chain elongation and is stabilized by S-phase checkpoint signalling
Sub types
  • Article
Ausgabe der Zeitschrift
29

Datenquelle: Web of Science (Lite)

Andere Metadatenquellen:
Autoren
  • Sarah Luke-Glaser
  • Brian Luke
  • Simona Grossi
  • Angelos Constantinou
DOI
10.1038/emboj.2009.371
eISSN
1460-2075
ISSN
0261-4189
Ausgabe der Veröffentlichung
4
Zeitschrift
The EMBO Journal
Online publication date
2009
Paginierung
795 - 805
Datum der Veröffentlichung
2010
Status
Published
Herausgeber
Springer Science and Business Media LLC
Herausgeber URL
http://dx.doi.org/10.1038/emboj.2009.371
Datum der Datenerfassung
2023
Titel
FANCM regulates DNA chain elongation and is stabilized by S-phase checkpoint signalling
Ausgabe der Zeitschrift
29

Datenquelle: Crossref

Abstract
FANCM binds and remodels replication fork structures in vitro. We report that in vivo, FANCM controls DNA chain elongation in an ATPase-dependent manner. In the presence of replication inhibitors that do not damage DNA, FANCM counteracts fork movement, possibly by remodelling fork structures. Conversely, through damaged DNA, FANCM promotes replication and recovers stalled forks. Hence, the impact of FANCM on fork progression depends on the underlying hindrance. We further report that signalling through the checkpoint effector kinase Chk1 prevents FANCM from degradation by the proteasome after exposure to DNA damage. FANCM also acts in a feedback loop to stabilize Chk1. We propose that FANCM is a ringmaster in the response to replication stress by physically altering replication fork structures and by providing a tight link to S-phase checkpoint signalling.
Addresses
  • Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, Epalinges s/Lausanne, Switzerland.
Autoren
  • Sarah Luke-Glaser
  • Brian Luke
  • Simona Grossi
  • Angelos Constantinou
DOI
10.1038/emboj.2009.371
eISSN
1460-2075
Externe Identifier
  • PubMed Identifier: 20010692
  • PubMed Central ID: PMC2829158
Funding acknowledgements
  • Swiss National Science Foundation: 118991
Open access
false
ISSN
0261-4189
Ausgabe der Veröffentlichung
4
Zeitschrift
The EMBO journal
Schlüsselwörter
  • Hela Cells
  • Humans
  • DNA Damage
  • Proteasome Endopeptidase Complex
  • DNA Helicases
  • Protein Kinases
  • RNA, Small Interfering
  • DNA
  • Signal Transduction
  • S Phase
  • DNA Repair
  • DNA Replication
  • Base Sequence
  • Models, Biological
  • Fanconi Anemia Complementation Group D2 Protein
  • Adenosine Triphosphatases
  • Checkpoint Kinase 1
Sprache
eng
Medium
Print-Electronic
Online publication date
2009
Paginierung
795 - 805
Datum der Veröffentlichung
2010
Status
Published
Datum der Datenerfassung
2009
Titel
FANCM regulates DNA chain elongation and is stabilized by S-phase checkpoint signalling.
Sub types
  • Research Support, Non-U.S. Gov't
  • research-article
  • Journal Article
Ausgabe der Zeitschrift
29

Datenquelle: Europe PubMed Central

Abstract
FANCM binds and remodels replication fork structures in vitro. We report that in vivo, FANCM controls DNA chain elongation in an ATPase-dependent manner. In the presence of replication inhibitors that do not damage DNA, FANCM counteracts fork movement, possibly by remodelling fork structures. Conversely, through damaged DNA, FANCM promotes replication and recovers stalled forks. Hence, the impact of FANCM on fork progression depends on the underlying hindrance. We further report that signalling through the checkpoint effector kinase Chk1 prevents FANCM from degradation by the proteasome after exposure to DNA damage. FANCM also acts in a feedback loop to stabilize Chk1. We propose that FANCM is a ringmaster in the response to replication stress by physically altering replication fork structures and by providing a tight link to S-phase checkpoint signalling.
Date of acceptance
2009
Autoren
  • Sarah Luke-Glaser
  • Brian Luke
  • Simona Grossi
  • Angelos Constantinou
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/20010692
DOI
10.1038/emboj.2009.371
eISSN
1460-2075
Externe Identifier
  • PubMed Central ID: PMC2829158
Ausgabe der Veröffentlichung
4
Zeitschrift
EMBO J
Schlüsselwörter
  • Adenosine Triphosphatases
  • Base Sequence
  • Checkpoint Kinase 1
  • DNA
  • DNA Damage
  • DNA Helicases
  • DNA Repair
  • DNA Replication
  • Fanconi Anemia Complementation Group D2 Protein
  • HeLa Cells
  • Humans
  • Models, Biological
  • Proteasome Endopeptidase Complex
  • Protein Kinases
  • RNA, Small Interfering
  • S Phase
  • Signal Transduction
Sprache
eng
Country
England
Paginierung
795 - 805
PII
emboj2009371
Datum der Veröffentlichung
2010
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
2010
Titel
FANCM regulates DNA chain elongation and is stabilized by S-phase checkpoint signalling.
Sub types
  • Journal Article
  • Research Support, Non-U.S. Gov't
Ausgabe der Zeitschrift
29

Datenquelle: PubMed

Abstract
FANCM binds and remodels replication fork structures in vitro. We report that in vivo, FANCM controls DNA chain elongation in an ATPase-dependent manner. In the presence of replication inhibitors that do not damage DNA, FANCM counteracts fork movement, possibly by remodelling fork structures. Conversely, through damaged DNA, FANCM promotes replication and recovers stalled forks. Hence, the impact of FANCM on fork progression depends on the underlying hindrance. We further report that signalling through the checkpoint effector kinase Chk1 prevents FANCM from degradation by the proteasome after exposure to DNA damage. FANCM also acts in a feedback loop to stabilize Chk1. We propose that FANCM is a ringmaster in the response to replication stress by physically altering replication fork structures and by providing a tight link to S-phase checkpoint signalling.
Autoren
  • Sarah Luke-Glaser
  • Brian Luke
  • Simona Grossi
  • Angelos Constantinou
DOI
10.1038/emboj.2009.371
Zeitschrift
The EMBO journal
Notes
keywords: Adenosine Triphosphatases/metabolism;Base Sequence;Checkpoint Kinase 1;DNA Damage;DNA Helicases/antagonists & inhibitors/genetics/metabolism;DNA Repair;DNA Replication/physiology;DNA/biosynthesis/genetics;Fanconi Anemia Complementation Group D2 Protein/antagonists & inhibitors/genetics/metabolism;HeLa Cells;Humans;Models, Biological;Proteasome Endopeptidase Complex/metabolism;Protein Kinases/metabolism;RNA, Small Interfering/genetics;S Phase;Signal Transduction
Artikelnummer
4
Paginierung
795 - 805
Datum der Veröffentlichung
2010
Datum der Datenerfassung
2023
Titel
FANCM regulates DNA chain elongation and is stabilized by S-phase checkpoint signalling
Sub types
  • article
Ausgabe der Zeitschrift
29

Datenquelle: Manual

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