A5073036493- Autophagy in Disease and Therapy
- Cellular transport and secretion
- Endoplasmic Reticulum Stress and Disease
- Calcium signaling and nucleotide metabolism
- Ubiquitin and proteasome pathways
- Mitochondrial Function and Pathology
- Lysosomal Storage Disorders Research
- Mosquito-borne diseases and control
- Cannabis and Cannabinoid Research
- Adenosine and Purinergic Signaling
- Glioma Diagnosis and Treatment
- Toxoplasma gondii Research Studies
- Extracellular vesicles in disease
- Epigenetics and DNA Methylation
- Immune Cell Function and Interaction
- Parkinson's Disease Mechanisms and Treatments
- Protein Kinase Regulation and GTPase Signaling
- RNA Interference and Gene Delivery
- CRISPR and Genetic Engineering
- Pancreatic function and diabetes
- Retinoids in leukemia and cellular processes
- Plant responses to water stress
- Histone Deacetylase Inhibitors Research
- T-cell and B-cell Immunology
- Lipid metabolism and biosynthesis
University of Oslo
2016-2025
Oslo University Hospital
2001-2025
Norwegian Cancer Society
1998-2024
Aarhus University
2018-2022
University of Copenhagen
2020
Faculty (United Kingdom)
2012-2015
Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences
2011-2015
Institute of Physiology and Basic Medicine
2011-2015
Washtenaw Community College
2012
University of Michigan–Ann Arbor
2012
Autophagy is involved with the turnover of intracellular components and management stress responses. Genetic studies in mice have shown that suppression neuronal autophagy can lead to accumulation protein aggregates neurodegeneration. However, no study has increasing autophagic gene expression be beneficial an aging nervous system. Here we demonstrate several genes reduced Drosophila neural tissues as a normal part aging. The age-dependent occurs concomitantly insoluble ubiquitinated...
The endosomal sorting complexes required for transport (ESCRTs) are to sort integral membrane proteins into intralumenal vesicles of the multivesicular body (MVB). Mutations in ESCRT-III subunit CHMP2B were recently associated with frontotemporal dementia and amyotrophic lateral sclerosis (ALS), neurodegenerative diseases characterized by abnormal ubiquitin-positive protein deposits affected neurons. We show here that autophagic degradation is inhibited cells depleted ESCRT subunits...
p62 has been proposed to mark ubiquitinated protein bodies for autophagic degradation. We report that the Drosophila melanogaster orthologue, Ref(2)P, is a regulator of aggregation in adult brain. demonstrate Ref(2)P localizes age-induced aggregates as well caused by reduced or proteasomal activity. A similar localization also observed D. models human neurodegenerative diseases. Although atg8a autophagy mutant flies show accumulation ubiquitin- and Ref(2)P-positive aggregates, this abrogated...
AbstractAccumulation of ubiquitinated proteins in cytoplasmic and/or nuclear inclusions is a hallmark several diseases associated with premature cell death. SQSTM1/p62 known to bind substrates and aid their aggregation degradation by macro-autophagy. We show here that p62 required recruit the large phosphoinositide-binding protein ALFY bodies generated upon amino acid starvation or puromycin-treatment. ALFY, as well p62, for formation autophagic ubiquitin-positive inclusions. Moreover, both...
The study of autophagy is rapidly expanding, and our knowledge the molecular mechanism its connections to a wide range physiological processes has increased substantially in past decade. vocabulary associated with grown concomitantly. In fact, it difficult for readers--even those who work field--to keep up ever-expanding terminology various autophagy-related processes. Accordingly, we have developed comprehensive glossary terms that meant provide quick reference researchers need brief...
Inactivation of the endosomal sorting complex required for transport (ESCRT) machinery has been reported to cause autophagic defects, but exact functions ESCRT proteins in macroautophagy/autophagy remain incompletely understood. Using live-cell fluorescence microscopy we found that filament-forming ESCRT-III subunit CHMP4B was recruited transiently nascent autophagosomes during starvation-induced autophagy and mitophagy, with residence times about 1 2 min, respectively. Correlative light...
Autophagy is a fundamental catabolic process that uses unique post-translational modification, the conjugation of ATG8 protein to phosphatidylethanolamine (PE). lipidation also occurs during non-canonical autophagy, parallel pathway involving single membranes (CASM) at endolysosomal compartments, with key functions in immunity, vision, and neurobiology. It widely assumed CASM involves same PE, but this has not been formally tested. Here, we discover all ATG8s can undergo alternative...
Phosphatidylinositol-3-phosphate [PtdIns(3)P] regulates endocytic and autophagic membrane traffic. In order to understand the downstream effects of PtdIns(3)P in these processes, it is important identify PtdIns(3)P-binding proteins, many which contain FYVE zinc-finger domains. Here, we describe a novel giant FYVE-domain-containing protein, named autophagy-linked protein (Alfy). Alfy ubiquitously expressed, shares sequence similarity with Chediak-Higashi-syndrome has putative homologues...
The fusion of transport vesicles with their cognate target membranes, an essential event in intracellular membrane trafficking, is regulated by SNARE proteins and Rab GTPases. GTPases are thought to act prior SNAREs vesicle docking, but the exact biochemical relationship between two classes molecules not known. We recently identified early endosomal autoantigen EEA1 as effector Rab5 endocytic fusion. Here we demonstrate that interacts directly specifically syntaxin-6, a implicated...