p62/SQSTM1 promotes mitophagy and activates the NRF2-mediated antioxidant and anti-inflammatory response restraining EBV-driven B lymphocyte proliferation

Roles of Inflammasomes in Epstein–Barr Virus-Associated Nasopharyngeal Cancer

(2021) Chin King Looi et al.   Cancers

DNA double-strand breaks induce H2Ax phosphorylation domains in a contact-dependent manner

(2020) Patrick L. Collins et al.   Nature Communications

Inhibition of PINK1/Parkin-dependent mitophagy sensitizes multidrug-resistant cancer cells to B5G1, a new betulinic acid analog

(2019) Nan Yao et al.   Cell Death & Disease

p62-mediated Selective autophagy endows virus-transformed cells with insusceptibility to DNA damage under oxidative stress

(2019) Ling Wang et al.   PLoS Pathogens

Nrf2 in cancers: A double‐edged sword

(2019) Shijia Wu et al.   Cancer Medicine

Mutant p53, Stabilized by Its Interplay with HSP90, Activates a Positive Feed-Back Loop Between NRF2 and p62 that Induces Chemo-Resistance to Apigenin in Pancreatic Cancer Cells

(2019) Maria Saveria Gilardini Montani et al.   Cancers

Epstein–Barr virus reprograms human B lymphocytes immediately in the prelatent phase of infection

(2019) Paulina Mrozek-Gorska et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Quercetin Interrupts the Positive Feedback Loop Between STAT3 and IL-6, Promotes Autophagy, and Reduces ROS, Preventing EBV-Driven B Cell Immortalization

(2019) Granato et al.   Biomolecules

Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis

(2018) Bernadette Carroll et al.   Nature Communications

EBV up-regulates PD-L1 on the surface of primary monocytes by increasing ROS and activating TLR signaling and STAT3

(2018) Maria Saveria Gilardini Montani et al.   JOURNAL OF LEUKOCYTE BIOLOGY

EBV reduces autophagy, intracellular ROS and mitochondria to impair monocyte survival and differentiation

(2018) M.S. Gilardini Montani et al.   Autophagy

p62/ SQSTM 1: ‘Jack of all trades’ in health and cancer

(2018) Pablo Sánchez‐Martín et al.   FEBS Journal

Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle

(2017) Pok Hau et al.   Viruses-Basel

ATM-deficiency increases genomic instability and metastatic potential in a mouse model of pancreatic cancer

(2017) Yiannis Drosos et al.   Scientific Reports

SQSTM1/p62 mediates crosstalk between autophagy and the UPS in DNA repair

(2016) Graeme Hewitt et al.   Autophagy

p62, Upregulated during Preneoplasia, Induces Hepatocellular Carcinogenesis by Maintaining Survival of Stressed HCC-Initiating Cells

(2016) Atsushi Umemura et al.   CANCER CELL

p62 in Cancer: Signaling Adaptor Beyond Autophagy

(2016) Jorge Moscat et al.   CELL

Chronic oxidative stress promotes H2AX protein degradation and enhances chemosensitivity in breast cancer patients

(2016) Tina Gruosso et al.   EMBO Molecular Medicine

Metabolic stress is a barrier to Epstein–Barr virus-mediated B-cell immortalization

(2016) Karyn McFadden et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Mitochondrial dynamics and viral infections: A close nexus

(2015) Mohsin Khan et al.   BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH

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

(2015) X Chen et al.   ONCOGENE

DNA Damage Signaling Is Induced in the Absence of Epstein—Barr Virus (EBV) Lytic DNA Replication and in Response to Expression of ZEBRA

(2015) Ruth Wang'ondu et al.   PLoS One

Metabolic Reprogramming of Stromal Fibroblasts through p62-mTORC1 Signaling Promotes Inflammation and Tumorigenesis

(2014) Tania Valencia et al.   CANCER CELL

Epstein-Barr Virus Essential Antigen EBNA3C Attenuates H2AX Expression

(2014) H. C. Jha et al.   JOURNAL OF VIROLOGY

Reactive Oxygen Species Production and Antioxidant Enzyme Expression after Epstein–Barr Virus Lytic Cycle Induction in Raji Cell Line

(2011) Bochra Gargouri et al.   BIOLOGICAL TRACE ELEMENT RESEARCH

Mitochondrial reactive oxygen species drive proinflammatory cytokine production: Figure 1.

(2011) Edwina Naik et al.   JOURNAL OF EXPERIMENTAL MEDICINE

An ATM/Chk2-Mediated DNA Damage-Responsive Signaling Pathway Suppresses Epstein-Barr Virus Transformation of Primary Human B Cells

(2010) Pavel A. Nikitin et al.   Cell Host & Microbe

p62 at the Crossroads of Autophagy, Apoptosis, and Cancer

(2009) Jorge Moscat et al.   CELL

Autophagy Suppresses Tumorigenesis through Elimination of p62

(2009) Robin Mathew et al.   CELL

MDM2-Dependent Inhibition of p53 Is Required for Epstein-Barr Virus B-Cell Growth Transformation and Infected-Cell Survival

(2009) E. Forte et al.   JOURNAL OF VIROLOGY

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

(2009) B Gruhne et al.   ONCOGENE

Copy number alterations of the H2AFX gene in sporadic breast cancer patients

(2008) Niloo Srivastava et al.   CANCER GENETICS AND CYTOGENETICS

Induction of Epstein-Barr virus (EBV) lytic cycle in vitro causes oxidative stress in lymphoblastoid B cell lines

(2008) Bochra Gargouri et al.   MOLECULAR AND CELLULAR BIOCHEMISTRY

Epstein-Barr virus induces an oxidative stress during the early stages of infection in B lymphocytes, epithelial, and lymphoblastoid cell lines

(2008) Saloua Lassoued et al.   MOLECULAR AND CELLULAR BIOCHEMISTRY