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WRNIP1 protects stalled forks from degradation and promotes fork restart after replication stress

The EMBO journal, 2016-07, Vol.35 (13), p.1437-1451

2016

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Rad52 prevents excessive replication fork reversal and protects from nascent strand degradation

Nature communications, 2019-03, Vol.10 (1), p.1412-1412, Article 1412

2019

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WRNIP1 prevents transcription-associated genomic instability

eLife, 2024-03, Vol.12

2024

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ATM pathway activation limits R-loop-associated genomic instability in Werner syndrome cells

Nucleic acids research, 2019-04, Vol.47 (7), p.3485

2019

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R-Loop-Associated Genomic Instability and Implication of WRN and WRNIP1

International journal of molecular sciences, 2022-01, Vol.23 (3), p.1547

2022

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ATR and ATM differently regulate WRN to prevent DSBs at stalled replication forks and promote replication fork recovery

The EMBO journal, 2010-09, Vol.29 (18), p.3156-3169

2010

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Physiological and Pathological Roles of RAD52 at DNA Replication Forks

Cancers, 2020-02, Vol.12 (2), p.402

2020

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RAD51 and mitotic function of mus81 are essential for recovery from low-dose of camptothecin in the absence of the WRN exonuclease

Nucleic acids research, 2019-07, Vol.47 (13), p.6796

2019

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Author Correction: Rad52 prevents excessive replication fork reversal and protects from nascent strand degradation

Nature communications, 2019-05, Vol.10 (1), p.2023-2023, Article 2023

2019

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CDK1 phosphorylates WRN at collapsed replication forks

Nature communications, 2016-09, Vol.7 (1), p.12880-15, Article 12880

2016

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Survival of the replication checkpoint deficient cells requires MUS81-RAD52 function

PLoS genetics, 2013-10, Vol.9 (10), p.e1003910

2013

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Understanding the molecular basis of common fragile sites instability: Role of the proteins involved in the recovery of stalled replication forks

Cell cycle (Georgetown, Tex.), 2011-12, Vol.10 (23), p.4039-4046

2011

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Werner syndrome helicase activity is essential in maintaining fragile site stability

The Journal of cell biology, 2008-01, Vol.180 (2), p.305-314

2008

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Replication fork stalling in WRN-deficient cells is overcome by prompt activation of a MUS81-dependent pathway

The Journal of cell biology, 2008-10, Vol.183 (2), p.241-252

2008

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Checkpoint Defects Elicit a WRNIP1-Mediated Response to Counteract R-Loop-Associated Genomic Instability

Cancers, 2020-02, Vol.12 (2), p.389

2020

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CSA and CSB play a role in the response to DNA breaks

Oncotarget, 2018-02, Vol.9 (14), p.11581-11591

2018

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Inducible SMARCAL1 knockdown in iPSC reveals a link between replication stress and altered expression of master differentiation genes

Disease models & mechanisms, 2019-10, Vol.12 (10)

2019

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BLM and the FANC proteins collaborate in a common pathway in response to stalled replication forks

The EMBO journal, 2004-08, Vol.23 (15), p.3154-3163

2004

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Werner's syndrome protein is phosphorylated in an ATR ATM-dependent manner following replication arrest and DNA damage induced during the S phase of the cell cycle

Oncogene, 2003-03, Vol.22 (10), p.1491-1500

2003

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Terminally differentiated muscle cells are defective in base excision DNA repair and hypersensitive to oxygen injury

Proceedings of the National Academy of Sciences - PNAS, 2007-10, Vol.104 (43), p.17010-17015

2007

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Replication fork recovery and regulation of common fragile sites stability

Cellular and molecular life sciences : CMLS, 2014-12, Vol.71 (23), p.4507-4517

2014

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Che-1 Promotes Tumor Cell Survival by Sustaining Mutant p53 Transcription and Inhibiting DNA Damage Response Activation

Cancer cell, 2010-08, Vol.18 (2), p.122-134

2010

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The mammalian mismatch repair protein MSH2 is required for correct MRE11 and RAD51 relocalization and for efficient cell cycle arrest induced by ionizing radiation in G2 phase

Oncogene, 2003-04, Vol.22 (14), p.2110-2120

2003

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Genome Instability at Common Fragile Sites: Searching for the Cause of Their Instability

BioMed research international, 2013-01, Vol.2013, p.730714-9

2013

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WRNIP1 protects stalled forks from degradation and promotes fork restart after replication stress

Rad52 prevents excessive replication fork reversal and protects from nascent strand degradation

WRNIP1 prevents transcription-associated genomic instability

ATM pathway activation limits R-loop-associated genomic instability in Werner syndrome cells

R-Loop-Associated Genomic Instability and Implication of WRN and WRNIP1

ATR and ATM differently regulate WRN to prevent DSBs at stalled replication forks and promote replication fork recovery

Physiological and Pathological Roles of RAD52 at DNA Replication Forks

Control of replication stress and mitosis in colorectal cancer stem cells through the interplay of PARP1, MRE11 and RAD51

RAD51 and mitotic function of mus81 are essential for recovery from low-dose of camptothecin in the absence of the WRN exonuclease

Author Correction: Rad52 prevents excessive replication fork reversal and protects from nascent strand degradation

CDK1 phosphorylates WRN at collapsed replication forks

Survival of the replication checkpoint deficient cells requires MUS81-RAD52 function

Understanding the molecular basis of common fragile sites instability: Role of the proteins involved in the recovery of stalled replication forks

Werner syndrome helicase activity is essential in maintaining fragile site stability

Replication fork stalling in WRN-deficient cells is overcome by prompt activation of a MUS81-dependent pathway

Checkpoint Defects Elicit a WRNIP1-Mediated Response to Counteract R-Loop-Associated Genomic Instability

CSA and CSB play a role in the response to DNA breaks

Inducible SMARCAL1 knockdown in iPSC reveals a link between replication stress and altered expression of master differentiation genes

BLM and the FANC proteins collaborate in a common pathway in response to stalled replication forks

Werner's syndrome protein is phosphorylated in an ATR ATM-dependent manner following replication arrest and DNA damage induced during the S phase of the cell cycle

Terminally differentiated muscle cells are defective in base excision DNA repair and hypersensitive to oxygen injury

Replication fork recovery and regulation of common fragile sites stability

Che-1 Promotes Tumor Cell Survival by Sustaining Mutant p53 Transcription and Inhibiting DNA Damage Response Activation

The mammalian mismatch repair protein MSH2 is required for correct MRE11 and RAD51 relocalization and for efficient cell cycle arrest induced by ionizing radiation in G2 phase

Genome Instability at Common Fragile Sites: Searching for the Cause of Their Instability

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