A5027596320- Cell death mechanisms and regulation
- Autophagy in Disease and Therapy
- Mitochondrial Function and Pathology
- interferon and immune responses
- RNA Interference and Gene Delivery
- Ubiquitin and proteasome pathways
- Inflammasome and immune disorders
- Phagocytosis and Immune Regulation
- Cancer-related Molecular Pathways
- ATP Synthase and ATPases Research
- Cancer Research and Treatments
- Endoplasmic Reticulum Stress and Disease
- NF-κB Signaling Pathways
- Immune Response and Inflammation
- Nanoplatforms for cancer theranostics
- Virus-based gene therapy research
- Protein Degradation and Inhibitors
- Multiple Myeloma Research and Treatments
- Glioma Diagnosis and Treatment
- Glycosylation and Glycoproteins Research
- Viral Infectious Diseases and Gene Expression in Insects
- RNA modifications and cancer
- Telomeres, Telomerase, and Senescence
- Protein Kinase Regulation and GTPase Signaling
- Extracellular vesicles in disease
University of Glasgow
2016-2025
Cancer Research UK
2014-2025
Cancer Research UK Scotland Institute
2015-2024
KU Leuven
2022
VIB-KU Leuven Center for Cancer Biology
2022
The Open University
2022
Betsi Cadwaladr University Health Board
2020
Institute of Cancer Research
2019
Institute of Cancer Research
2014
Glasgow Life
2014
Cell senescence is an important tumour suppressor mechanism and driver of ageing. Both functions are dependent on the development senescent phenotype, which involves overproduction pro-inflammatory pro-oxidant signals. However, exact mechanisms regulating these phenotypes remain poorly understood. Here, we show critical role mitochondria in cellular senescence. In multiple models senescence, absence reduced a spectrum effectors while preserving ATP production via enhanced glycolysis. Global...
Article26 July 2018Open Access Source DataTransparent process Mitochondrial inner membrane permeabilisation enables mtDNA release during apoptosis Joel S Riley orcid.org/0000-0001-9170-5716 Cancer Research UK Beatson Institute, Glasgow, Institute of Sciences, University Search for more papers by this author Giovanni Quarato orcid.org/0000-0003-1167-3422 Department Immunology, St. Jude Children's Hospital, Memphis, TN, USA Catherine Cloix Jonathan Lopez orcid.org/0000-0003-3768-2378 Jim...
During apoptosis, the mitochondrial outer membrane is permeabilized, leading to release of cytochrome c that activates downstream caspases. Mitochondrial permeabilization (MOMP) has historically been thought occur synchronously and completely throughout a cell, rapid caspase activation apoptosis. Using new imaging approach, we demonstrate MOMP not an all-or-nothing event. Rather, find minority mitochondria can undergo in stress-regulated manner, phenomenon term "minority MOMP." Crucially,...
Abstract Senescent cells drive age-related tissue dysfunction partially through the induction of a chronic senescence-associated secretory phenotype (SASP) 1 . Mitochondria are major regulators SASP; however, underlying mechanisms have not been elucidated 2 often essential for apoptosis, cell fate distinct from cellular senescence. During widespread mitochondrial outer membrane permeabilization (MOMP) commits to die 3 Here we find that MOMP occurring in subset mitochondria is feature This...
Programmed necrosis (or necroptosis) is a form of cell death triggered by the activation receptor interacting protein kinase-3 (RIPK3). Several reports have implicated mitochondria and mitochondrial reactive oxygen species (ROS) generation as effectors RIPK3-dependent death. Here, we directly test this idea employing method for specific removal via mitophagy. Mitochondria-deficient cells were resistant to pathway apoptosis, but efficiently died tumor factor (TNF)-induced, programmed or...
Mitophagy is an evolutionarily conserved process that selectively targets impaired mitochondria for degradation. Defects in mitophagy are often associated with diverse pathologies, including cancer. Because the main known regulators of frequently inactivated cancer cells, mechanisms regulate cells not fully understood. Here, we identified E3 ubiquitin ligase (ARIH1/HHARI) triggers a PINK1-dependent manner. We found ARIH1/HHARI polyubiquitinates damaged mitochondria, leading to their removal...