A5051174345- Mitochondrial Function and Pathology
- Adipose Tissue and Metabolism
- Cancer, Hypoxia, and Metabolism
- ATP Synthase and ATPases Research
- Metabolism and Genetic Disorders
- Ubiquitin and proteasome pathways
- Endoplasmic Reticulum Stress and Disease
- Lipid metabolism and biosynthesis
- Metabolomics and Mass Spectrometry Studies
- Autophagy in Disease and Therapy
- Pancreatic function and diabetes
- Click Chemistry and Applications
- Computational Drug Discovery Methods
- Liver Disease Diagnosis and Treatment
- Retinoids in leukemia and cellular processes
- Peroxisome Proliferator-Activated Receptors
- Metabolism, Diabetes, and Cancer
- Epigenetics and DNA Methylation
- Cardiovascular Function and Risk Factors
- Heme Oxygenase-1 and Carbon Monoxide
- Cancer Research and Treatment
- 14-3-3 protein interactions
- Biological Research and Disease Studies
- Muscle Physiology and Disorders
- Telomeres, Telomerase, and Senescence
Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas
2008-2025
Instituto de Salud Carlos III
2010-2025
Institut de Biologia Molecular de Barcelona
2022-2025
University of California, Los Angeles
2016-2024
Boston University
2010-2019
Diabetes Australia
2019
Ben-Gurion University of the Negev
2018
Oklahoma State University Center for Health Sciences
2018
Boston Medical Center
2010-2014
Northwestern University
2013
Macroautophagy (autophagy) is a regulated catabolic pathway to degrade cellular organelles and macromolecules. The role of autophagy in cancer complex may differ depending on tumor type or context. Here we show that pancreatic cancers have distinct dependence autophagy. Pancreatic primary tumors cell lines elevated under basal conditions. Genetic pharmacologic inhibition leads increased reactive oxygen species, DNA damage, metabolic defect leading decreased mitochondrial oxidative...
Mitochondria are dynamic organelles that play a key role in energy conversion. Optimal mitochondrial function is ensured by quality-control system tightly coupled to fusion and fission. In this connection, mitofusin 2 (Mfn2) participates undergoes repression muscle from obese or type diabetic patients. Here, we provide vivo evidence Mfn2 plays an essential metabolic homeostasis. Liver-specific ablation of mice led numerous abnormalities, characterized glucose intolerance enhanced hepatic...
Mitochondrial dysfunction and oxidative damage induced by bactericidal antibiotics in mammalian cells may be alleviated an antioxidant or prevented preferential use of bacteriostatic antibiotics.
Mitofusin-2 (Mfn2) is a mitochondrial membrane protein that participates in fusion mammalian cells and mutations the Mfn2 gene cause Charcot–Marie–Tooth neuropathy type 2A. Here, we show loss-of-function inhibits pyruvate, glucose fatty acid oxidation reduces potential, whereas gain-of-function increases potential. As to mechanisms involved, have found represses nuclear-encoded subunits of OXPHOS complexes I, II, III V, overexpression induced IV V. Obesity-induced deficiency rat skeletal...
Mitofusin 2 (Mfn2) is a mitochondrial membrane protein that participates in fusion and regulates metabolism mammalian cells. Here, we show Mfn2 gene expression induced skeletal muscle brown adipose tissue by conditions associated with enhanced energy expenditure, such as cold exposure or beta(3)-adrenergic agonist treatment. In keeping the role of peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1 alpha on demonstrate stimulatory effect PGC-1 mRNA also stimulated activity...
Article14 October 2019Open Access Source DataTransparent process Individual cristae within the same mitochondrion display different membrane potentials and are functionally independent Dane M Wolf Department of Medicine (Endocrinology), Molecular Medical Pharmacology, David Geffen School Medicine, University California, Los Angeles, CA, USA Graduate Program in Nutrition Metabolism, Sciences, Boston Boston, MA, Search for more papers by this author Mayuko Segawa Arun Kumar Kondadi Institute...
Resource20 May 2020Open Access Source DataTransparent process A novel approach to measure mitochondrial respiration in frozen biological samples Rebeca Acin-Perez Corresponding Author [email protected] orcid.org/0000-0001-9553-8337 Department of Medicine, Endocrinology, David Geffen School University California, Los Angeles, CA, USA Metabolism Theme, Search for more papers by this author Ilan Y Benador Nutrition and Metabolism, Graduate Medical Sciences, Boston Boston, MA, Anton Petcherski...
Article18 February 2020Open Access Transparent process Cristae undergo continuous cycles of membrane remodelling in a MICOS-dependent manner Arun Kumar Kondadi orcid.org/0000-0002-5888-7834 Institute Biochemistry and Molecular Biology I, Medical Faculty, Heinrich Heine University Düsseldorf, Germany Search for more papers by this author Ruchika Anand orcid.org/0000-0001-7337-6007 Sebastian Hänsch Faculty Mathematics Natural Sciences, Center Advanced Imaging, Jennifer Urbach...
Changes in mitochondrial morphology are associated with nutrient utilization, but the precise causalities and underlying mechanisms remain unknown. Here, using cellular models representing a wide variety of shapes, we show strong linear correlation between fragmentation increased fatty acid oxidation (FAO) rates. Forced elongation following MFN2 over-expression or DRP1 depletion diminishes FAO, while forced upon knockdown knockout augments FAO as evident from respirometry metabolic tracing....
Non-alcoholic fatty liver disease (NAFLD) is the most common in world. High levels of free acids impair hepatic lysosomal acidification and reduce autophagic flux. We investigate whether restoration function NAFLD recovers flux, mitochondrial function, insulin sensitivity. Here, we report synthesis novel biodegradable acid-activated acidifying nanoparticles (acNPs) as a lysosome targeting treatment to restore acidity autophagy. The acNPs, composed fluorinated polyesters, remain inactive at...
OBJECTIVE Type 2 diabetes is associated with insulin resistance and skeletal muscle mitochondrial dysfunction. We have found that subjects early-onset type show incapacity to increase Vo2max in response chronic exercise. This suggests a defect Here, we explored the nature of mechanisms involved. RESEARCH DESIGN AND METHODS Muscle biopsies were collected from young diabetic obese control before after acute or exercise protocols, expression genes and/or proteins relevant function was measured....
Abstract Macroautophagy (autophagy) is a critical cellular stress response; however, the signal transduction pathways controlling autophagy induction in response to are poorly understood. Here we reveal new mechanism of control whose deregulation disrupts mitochondrial integrity and energy homeostasis vivo . Stress conditions including hypoxia exercise induce reactive oxygen species (ROS) through upregulation protein complex involving REDD1, an mTORC1 inhibitor pro-oxidant TXNIP. Decreased...
Background There is no evidence to date on whether transcriptional regulators are able shift the balance between mitochondrial fusion and fission events through selective control of gene expression. Methodology/Principal Findings Here, we demonstrate that reduced size observed in knock-out mice for regulator PGC-1β associated with a reduction Mitofusin 2 (Mfn2) expression, protein. This decrease Mfn2 specific since expression remaining components machinery were not affected. Furthermore,...