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Herpesvirus ubiquitin deconjugases

Seminars in cell & developmental biology, 2022-12, Vol.132, p.185-192

Masucci, Maria G.

2022

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14-3-3 scaffold proteins mediate the inactivation of trim25 and inhibition of the type I interferon response by herpesvirus deconjugases

PLoS pathogens, 2019-11, Vol.15 (11), p.e1008146-e1008146

2019

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The Epstein-Barr virus deubiquitinase BPLF1 targets SQSTM1/p62 to inhibit selective autophagy

Autophagy, 2021-11, Vol.17 (11), p.3461-3474

2021

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Inhibition of selective autophagy by members of the herpesvirus ubiquitin-deconjugase family

Biochemical journal, 2021-06, Vol.478 (12), p.2297-2308

2021

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Three Epstein-Barr virus latency proteins independently promote genomic instability by inducing DNA damage, inhibiting DNA repair and inactivating cell cycle checkpoints

Oncogene, 2009-11, Vol.28 (45), p.3997-4008

2009

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The Epstein-Barr virus nuclear antigen-1 upregulates the cellular antioxidant defense to enable B-cell growth transformation and immortalization

Oncogene, 2020-01, Vol.39 (3), p.603-616

2020

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Herpesvirus deconjugases inhibit the IFN response by promoting TRIM25 autoubiquitination and functional inactivation of the RIG-I signalosome

PLoS pathogens, 2018-01, Vol.14 (1), p.e1006852-e1006852

2018

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Remodeling of the ribosomal quality control and integrated stress response by viral ubiquitin deconjugases

Nature communications, 2023-12, Vol.14 (1), p.8315-8315, Article 8315

2023

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The Epstein-Barr virus miR-BHRF1-1 targets RNF4 during productive infection to promote the accumulation of SUMO conjugates and the release of infectious virus

PLoS pathogens, 2017-04, Vol.13 (4), p.e1006338-e1006338

2017

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Oxidative stress enables Epstein-Barr virus-induced B-cell transformation by posttranscriptional regulation of viral and cellular growth-promoting factors

Oncogene, 2016-07, Vol.35 (29), p.3807-3816

2016

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Viral Ubiquitin and Ubiquitin-Like Deconjugases—Swiss Army Knives for Infection

Biomolecules (Basel, Switzerland), 2020-08, Vol.10 (8), p.1137

Masucci, Maria Grazia

2020

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Telomere dysfunction and activation of alternative lengthening of telomeres in B-lymphocytes infected by Epstein-Barr virus

Oncogene, 2013-12, Vol.32 (49), p.5522-5530

2013

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The Epstein-Barr virus deubiquitinating enzyme BPLF1 regulates the activity of topoisomerase II during productive infection

PLoS pathogens, 2021-09, Vol.17 (9), p.e1009954-e1009954

2021

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Caspase-1 promotes Epstein-Barr virus replication by targeting the large tegument protein deneddylase to the nucleus of productively infected cells

PLoS pathogens, 2013-10, Vol.9 (10), p.e1003664-e1003664

2013

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Epstein-Barr virus nuclear antigen-1 promotes genomic instability via induction of reactive oxygen species

Proceedings of the National Academy of Sciences - PNAS, 2009-02, Vol.106 (7), p.2313-2318

2009

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The Epstein-Barr virus nuclear antigen-1 promotes telomere dysfunction via induction of oxidative stress

Leukemia, 2011-06, Vol.25 (6), p.1017-1025

2011

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Chronic exposure to the cytolethal distending toxins of Gram‐negative bacteria promotes genomic instability and altered DNA damage response

Cellular microbiology, 2013-01, Vol.15 (1), p.98-113

2013

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Infection with genotoxin‐producing Salmonella enterica synergises with loss of the tumour suppressor APC in promoting genomic instability via the PI3K pathway in colonic epithelial cells

Cellular microbiology, 2019-12, Vol.21 (12), p.e13099-n/a

2019

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Correction: The Epstein-Barr virus nuclear antigen-1 upregulates the cellular antioxidant defense to enable B-cell growth transformation and immortalization

Oncogene, 2020-02, Vol.39 (9), p.2028-2028

2020

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A bacterial genotoxin causes virus reactivation and genomic instability in Epstein–Barr virus infected epithelial cells pointing to a role of co‐infection in viral oncogenesis

International journal of cancer, 2019-01, Vol.144 (1), p.98-109

2019

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Interaction With 14-3-3 Correlates With Inactivation of the RIG-I Signalosome by Herpesvirus Ubiquitin Deconjugases

Frontiers in immunology, 2020-03, Vol.11, p.437-437

2020

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Regulation of Telomere Homeostasis during Epstein-Barr virus Infection and Immortalization

Viruses, 2017-08, Vol.9 (8), p.217

2017

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The translation initiation factor 3f (eIF3f) exhibits a deubiquitinase activity regulating Notch activation

PLoS biology, 2010-11, Vol.8 (11), p.e1000545-e1000545

2010

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A deneddylase encoded by Epstein-Barr virus promotes viral DNA replication by regulating the activity of cullin-RING ligases

Nature cell biology, 2010-04, Vol.12 (4), p.351-361

2010

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The ER-resident ubiquitin-specific protease 19 participates in the UPR and rescues ERAD substrates

EMBO reports, 2009-07, Vol.10 (7), p.755-761

2009

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Herpesvirus ubiquitin deconjugases

14-3-3 scaffold proteins mediate the inactivation of trim25 and inhibition of the type I interferon response by herpesvirus deconjugases

The Epstein-Barr virus deubiquitinase BPLF1 targets SQSTM1/p62 to inhibit selective autophagy

Inhibition of selective autophagy by members of the herpesvirus ubiquitin-deconjugase family

Three Epstein-Barr virus latency proteins independently promote genomic instability by inducing DNA damage, inhibiting DNA repair and inactivating cell cycle checkpoints

The Epstein-Barr virus nuclear antigen-1 upregulates the cellular antioxidant defense to enable B-cell growth transformation and immortalization

Herpesvirus deconjugases inhibit the IFN response by promoting TRIM25 autoubiquitination and functional inactivation of the RIG-I signalosome

Remodeling of the ribosomal quality control and integrated stress response by viral ubiquitin deconjugases

The Epstein-Barr virus miR-BHRF1-1 targets RNF4 during productive infection to promote the accumulation of SUMO conjugates and the release of infectious virus

Oxidative stress enables Epstein-Barr virus-induced B-cell transformation by posttranscriptional regulation of viral and cellular growth-promoting factors

Viral Ubiquitin and Ubiquitin-Like Deconjugases—Swiss Army Knives for Infection

Telomere dysfunction and activation of alternative lengthening of telomeres in B-lymphocytes infected by Epstein-Barr virus

The Epstein-Barr virus deubiquitinating enzyme BPLF1 regulates the activity of topoisomerase II during productive infection

Caspase-1 promotes Epstein-Barr virus replication by targeting the large tegument protein deneddylase to the nucleus of productively infected cells

Epstein-Barr virus nuclear antigen-1 promotes genomic instability via induction of reactive oxygen species

The Epstein-Barr virus nuclear antigen-1 promotes telomere dysfunction via induction of oxidative stress

Chronic exposure to the cytolethal distending toxins of Gram‐negative bacteria promotes genomic instability and altered DNA damage response

Infection with genotoxin‐producing Salmonella enterica synergises with loss of the tumour suppressor APC in promoting genomic instability via the PI3K pathway in colonic epithelial cells

Correction: The Epstein-Barr virus nuclear antigen-1 upregulates the cellular antioxidant defense to enable B-cell growth transformation and immortalization

A bacterial genotoxin causes virus reactivation and genomic instability in Epstein–Barr virus infected epithelial cells pointing to a role of co‐infection in viral oncogenesis

Interaction With 14-3-3 Correlates With Inactivation of the RIG-I Signalosome by Herpesvirus Ubiquitin Deconjugases

Regulation of Telomere Homeostasis during Epstein-Barr virus Infection and Immortalization

The translation initiation factor 3f (eIF3f) exhibits a deubiquitinase activity regulating Notch activation

A deneddylase encoded by Epstein-Barr virus promotes viral DNA replication by regulating the activity of cullin-RING ligases

The ER-resident ubiquitin-specific protease 19 participates in the UPR and rescues ERAD substrates

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