A5030491036- Mitochondrial Function and Pathology
- Gut microbiota and health
- Genetic Neurodegenerative Diseases
- Metabolism, Diabetes, and Cancer
- Metabolism and Genetic Disorders
- Helicobacter pylori-related gastroenterology studies
- Diet and metabolism studies
- Metalloenzymes and iron-sulfur proteins
- Amyotrophic Lateral Sclerosis Research
- Hereditary Neurological Disorders
- Peripheral Neuropathies and Disorders
- Medical Imaging and Pathology Studies
- Autophagy in Disease and Therapy
- Genomics and Rare Diseases
- Religion, Spirituality, and Psychology
- Cannabis and Cannabinoid Research
- Terrorism, Counterterrorism, and Political Violence
- Cellular transport and secretion
University Medical Center of the Johannes Gutenberg University Mainz
2021-2024
Johannes Gutenberg University Mainz
2021-2024
Institute for Molecular Medicine
2024
American University of Beirut
2019-2023
Institute of Molecular Biology
2021
Institute of Molecular Medicine
2021
Diabetic dysbiosis has been described as a novel key player in diabetes and diabetic complications. However, the cellular/molecular alterations associated with remain poorly characterized. For that, control, non-obese type 2 MKR mice treated butyrate were used to delineate epigenetic, cellular molecular mechanisms by which induces colon shortening inflammation attesting gastrointestinal disturbance. Our results show that is T2DM characterized reduced Bacteroid fragilis population...
Ion transport within mitochondria influences their structure, energy production, and cell death regulation. TMBIM5, a conserved calcium/proton exchanger in the inner mitochondrial membrane, contributes to ATP synthesis, apoptosis The relationship of TMBIM5 with calcium uniporter complex formed by MCU, MICU1-3, EMRE remains undefined. We generated Tmbim5-deficient Drosophila that exhibit disrupted cristae architecture, premature permeability transition pore opening, reduced uptake, swelling -...
Charcot-Marie-Tooth (CMT) disease 4A is an autosomal-recessive polyneuropathy caused by mutations of ganglioside-induced differentiation-associated protein 1 (GDAP1), a putative glutathione transferase, which affects mitochondrial shape and alters cellular Ca2+ homeostasis. Here, we identify the underlying mechanism. We found that patient-derived motoneurons GDAP1 knockdown SH-SY5Y cells display two phenotypes: more tubular mitochondria metabolism characterized glutamine dependence fewer...
Parkinson’s disease (PD) is characterized by the progressive loss of dopaminergic neurons in substantia nigra midbrain. Familial cases PD are often caused mutations PTEN-induced kinase 1 (PINK1) and ubiquitin ligase Parkin, both pivotal maintaining mitochondrial quality control. CISD1, a homodimeric iron-sulfur-binding protein, major target Parkin-mediated ubiquitination. We here discovered heightened propensity CISD1 to form dimers Pink1 mutant flies from PINK1 mutation patients. The dimer...
e15505 Background: Gut microbiota favors butyrate-forming bacteria and maintains homeostatic balance which is revoked during the development of colorectal cancer (CRC)-associated dysbiosis. Butyrate a short chain fatty acid that acts as lysine deacetylase inhibitor known to activate AMPK pathway well inhibiting inflammation ROS production. The role activation in diabetes-associated complications including poorly understood. This project examines dysbiosis butyrate on CRC onset disease...
Abstract Parkinson’s disease (PD) is characterized by the progressive loss of dopaminergic neurons in substantia nigra midbrain. Familial cases PD are often caused mutations PTEN-induced kinase 1 (PINK1) and ubiquitin ligase Parkin, both pivotal maintaining mitochondrial quality control. CISD1, a homodimeric iron-sulfur-binding protein, major target Parkin-mediated ubiquitination. We here discovered heightened propensity CISD1 to form dimers Pink1 mutant flies from PINK1 mutation patients....
Abstract Charcot-Marie-Tooth (CMT) disease 4A is an autosomal-recessive polyneuropathy caused by mutations of ganglioside-induced differentiation-associated protein 1 (GDAP1), a putative glutathione transferase, which affects mitochondrial shape and alters cellular calcium homeostasis. Here, we identify the underlying mechanism. We found that patient-derived motoneurons GDAP1 knockdown SH-SY5Y cells display two phenotypes: more tubular mitochondria metabolism characterized glutamine...
Abstract Charcot-Marie-Tooth (CMT) disease 4A is an autosomal-recessive polyneuropathy caused by mutations of ganglioside-induced differentiation-associated protein 1 (GDAP1), a putative glutathione transferase, which affects mitochondrial shape and alters cellular Ca 2+ homeostasis. Here, we identify the underlying mechanism. We found that patient-derived motoneurons GDAP1 knockdown SH-SY5Y cells display two phenotypes: more tubular mitochondria metabolism characterized glutamine dependence...