Hans Zischka

ORCID: 0000-0002-4047-1566
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • Trace Elements in Health
  • Heavy Metal Exposure and Toxicity
  • Drug Transport and Resistance Mechanisms
  • Liver Disease Diagnosis and Treatment
  • Metabolism and Genetic Disorders
  • Metabolomics and Mass Spectrometry Studies
  • Iron Metabolism and Disorders
  • ATP Synthase and ATPases Research
  • Adipose Tissue and Metabolism
  • Endoplasmic Reticulum Stress and Disease
  • Cancer, Hypoxia, and Metabolism
  • Aluminum toxicity and tolerance in plants and animals
  • Selenium in Biological Systems
  • Intellectual Property and Patents
  • Neuroscience and Neuropharmacology Research
  • Ubiquitin and proteasome pathways
  • Cell death mechanisms and regulation
  • Redox biology and oxidative stress
  • Ion channel regulation and function
  • Diet, Metabolism, and Disease
  • Autophagy in Disease and Therapy
  • Innovation Policy and R&D
  • Effects of Radiation Exposure
  • Advanced Proteomics Techniques and Applications

Technical University of Munich
2014-2025

Helmholtz Zentrum München
2016-2025

Institute of Bioinformatics and Systems Biology
2002-2019

Medical University of Vienna
2019

University of Amsterdam
2011

Amsterdam UMC Location University of Amsterdam
2011

Ludwig-Maximilians-Universität München
2003-2011

Center for Environmental Health
2011

German Center for Infection Research
2010

Institute of Groundwater Ecology
2002-2008

In this study yeast mitochondria were used as a model system to apply, evaluate, and integrate different genomic approaches define the proteins of an organelle. Liquid chromatography mass spectrometry applied purified identified 546 proteins. By expression analysis comparison other proteome studies, we demonstrate that proteomic approach identifies primarily highly abundant expanding our evaluation types approaches, including systematic deletion phenotype screening, profiling, subcellular...

10.1371/journal.pbio.0020160 article EN cc-by PLoS Biology 2004-06-09

Wilson disease (WD) is a rare hereditary condition that caused by genetic defect in the copper-transporting ATPase ATP7B results hepatic copper accumulation and lethal liver failure. The present study focuses on structural mitochondrial alterations precede clinical symptoms livers of rats lacking Atp7b, an animal model for WD. Liver mitochondria from these Atp7b–/– contained enlarged cristae widened intermembrane spaces, which coincided with massive copper. These changes, however, preceded...

10.1172/jci45401 article EN Journal of Clinical Investigation 2011-03-02

Backround Radiation therapy treatment of breast cancer, Hodgkin's disease or childhood cancers expose the heart to high local radiation doses, causing an increased risk cardiovascular in survivors decades after treatment. The mechanisms that underlie damage remain poorly understood so far. Previous data show impairment mitochondrial oxidative metabolism is directly linked development disease. Methodology/Principal findings In this study, radiation-induced vivo effects on cardiac proteome and...

10.1371/journal.pone.0027811 article EN cc-by PLoS ONE 2011-12-08

In Wilson disease (WD), functional loss of ATPase copper-transporting β (ATP7B) impairs biliary copper excretion, leading to excessive accumulation in the liver and fulminant hepatitis. Current US Food Drug Administration- European Medicines Agency-approved pharmacological treatments usually fail restore homeostasis patients with WD who have progressed acute failure, leaving transplantation as only viable treatment option. Here, we investigated therapeutic utility methanobactin (MB), a...

10.1172/jci85226 article EN Journal of Clinical Investigation 2016-06-19

SummaryPatients with non-small cell lung cancer (NSCLC) are routinely treated cytotoxic agents such as cisplatin. Through a genome-wide siRNA-based screen, we identified vitamin B6 metabolism central regulator of cisplatin responses in vitro and vivo. By aggravating bioenergetic catastrophe that involves the depletion intracellular glutathione, exacerbates cisplatin-mediated DNA damage, thus sensitizing large panel lines to apoptosis. Moreover, sensitizes cells apoptosis induction by...

10.1016/j.celrep.2012.06.017 article EN cc-by-nc-nd Cell Reports 2012-07-26

Mg2+ regulates many physiological processes and signalling pathways. However, little is known about the mechanisms underlying organismal balance of Mg2+. Capitalizing on a set newly generated mouse models, we provide an integrated mechanistic model regulation during prenatal development in adult mice by ion channel TRPM6. We show that TRPM6 activity placenta yolk sac essential for embryonic development. In mice, required intestine to maintain balance, but dispensable kidney. Trpm6...

10.7554/elife.20914 article EN cc-by eLife 2016-12-19

Ferroptosis is a regulated cell death modality that occurs upon iron-dependent lipid peroxidation. Recent research has identified many regulators induce or inhibit ferroptosis; yet, regulatory processes and networks remain to be elucidated. In this study, we performed chemical genetics screen using small molecules with known mode of action two agonists the nuclear receptor Farnesoid X Receptor (FXR) suppress ferroptosis, but not apoptosis necroptosis. We demonstrate in liver cells high FXR...

10.1038/s41467-023-42702-8 article EN cc-by Nature Communications 2023-10-30

Selenium homeostasis depends on hepatic biosynthesis of selenoprotein P (SELENOP) and SELENOP-mediated transport from the liver to e.g. brain. In addition, maintains copper homeostasis. metabolism are inversely regulated, as increasing decreasing selenium levels observed in blood during aging inflammation. Here we show that treatment increased intracellular SELENOP hepatocytes decreased extracellular levels. Hepatic accumulation is a characteristic Wilson's disease. Accordingly, were low...

10.1038/s41467-023-39245-3 article EN cc-by Nature Communications 2023-06-13

Excess copper causes hepatocyte death in hereditary Wilson's disease (WD). Current WD treatments by copper-binding chelators may gradually reduce overload; they fail, however, to bring hepatic close normal physiological levels. Consequently, lifelong daily dose regimens are required hinder progression. This result severe issues due nonadherence or unwanted adverse drug reactions and also switching ultimate treatment failures. study comparatively tested bacteria-derived binding...

10.1053/j.gastro.2023.03.216 article EN cc-by-nc-nd Gastroenterology 2023-03-24

Abstract The analysis of complex cellular proteomes by means two‐dimensional gel electrophoresis (2‐DE) is significantly limited the power resolution this technique. Although subcellular fractionation can be a fundamental first step to increase resolution, it frequently leads preparations contaminated with other structures. Here, we chose mitochondria Saccharomyces cerevisiae demonstrate that an integrated zone‐electrophoretic purification (ZE), free‐flow device (FFE), assist in overcoming...

10.1002/pmic.200300376 article EN PROTEOMICS 2003-06-01
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