Stephan M. Huber

ORCID: 0000-0002-9430-8334
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About
Contact & Profiles
Research Areas
  • Erythrocyte Function and Pathophysiology
  • Ion channel regulation and function
  • Ion Transport and Channel Regulation
  • Calcium signaling and nucleotide metabolism
  • Neonatal Health and Biochemistry
  • Blood properties and coagulation
  • Neuroscience and Neuropharmacology Research
  • Lipid Membrane Structure and Behavior
  • Hemoglobinopathies and Related Disorders
  • Glioma Diagnosis and Treatment
  • Malaria Research and Control
  • Cell death mechanisms and regulation
  • Renal and related cancers
  • Cardiac electrophysiology and arrhythmias
  • Immunotherapy and Immune Responses
  • Mitochondrial Function and Pathology
  • Nicotinic Acetylcholine Receptors Study
  • Phagocytosis and Immune Regulation
  • Ion Channels and Receptors
  • Cancer, Hypoxia, and Metabolism
  • Toxin Mechanisms and Immunotoxins
  • Neuroscience and Neural Engineering
  • Cancer-related Molecular Pathways
  • CAR-T cell therapy research
  • Venomous Animal Envenomation and Studies

University of Tübingen
2015-2025

University Children's Hospital Tübingen
1993-2024

University of Teacher Education Zug
2019

German Cancer Research Center
2017

Heidelberg University
1998-2017

Technical University of Munich
1993-2011

Radiation Oncology Associates
2010

Czech Academy of Sciences, Institute of Physiology
1993-2008

TH Bingen University of Applied Sciences
2007

University of Helsinki
2005

Exposure of erythrocytes to the Ca2+ ionophore ionomycin has recently been shown induce cell shrinkage, membrane blebbing, and breakdown phosphatidylserine asymmetry, all features typical apoptosis nucleated cells. Although asymmetry is thought result from activation a Ca2+-sensitive scramblase, mechanism role shrinkage have not explored. The present study was performed test whether ionomycin-induced Gardos K+ channels subsequent participate in human erythrocytes. According on-cell...

10.1152/ajpcell.00186.2003 article EN AJP Cell Physiology 2003-12-01

Paroxysmal dyskinesias are episodic movement disorders that can be inherited or sporadic in nature. The pathophysiology underlying these remains largely unknown but may involve disrupted ion homeostasis due to defects cell-surface channels nutrient transporters. In this study, we describe a family with paroxysmal exertion-induced dyskinesia (PED) over 3 generations. Their PED was accompanied by epilepsy, mild developmental delay, reduced CSF glucose levels, hemolytic anemia echinocytosis,...

10.1172/jci34438 article EN Journal of Clinical Investigation 2008-04-30

Exposure of erythrocytes to osmotic shock, oxidative stress, and energy depletion activates Cl--sensitive Ca2+-permeable cation channels. Subsequent Ca2+ entry triggers eryptosis, characterized by erythrocyte shrinkage, membrane blebbing, phosphatidylserine exposure all features typical for apoptotic death nucleated cells. Erythrocytes exposing are recognized, bound, engulfed, degraded macrophages. Eryptosis thus fosters clearance affected from circulating blood. Iron deficiency leads...

10.1096/fj.05-4872fje article EN The FASEB Journal 2005-12-21

Oxidative stress induces complex alterations of membrane proteins in red blood cells (RBCs) eventually leading to haemolysis. To study changes ion permeability induced by oxidative stress, whole‐cell patch‐clamp recordings and haemolysis experiments were performed control oxidised human RBCs. Control RBCs exhibited a small cation‐selective conductance (236 ± 38 pS; n = 8) which was highly sensitive the external Cl − concentration: replacement NaCl bath sodium gluconate an increase this...

10.1113/jphysiol.2001.013040 article EN The Journal of Physiology 2002-03-01

Glucose depletion of erythrocytes leads to activation Ca2+-permeable cation channels, Ca2+ entry, a Ca2+-sensitive erythrocyte scramblase, and subsequent exposure phosphatidylserine at the surface. entry into was previously shown be stimulated by phorbol esters inhibited staurosporine chelerythrine is thus thought regulated protein phosphorylation/dephosphorylation, presumably via kinase C (PKC) corresponding phosphoserine/threonine phosphatases. The present experiments explored whether PKC...

10.1152/ajpcell.00283.2005 article EN AJP Cell Physiology 2005-12-07

Erythrocyte diseases such as sickle cell anemia, thalassemia and glucose-6-phosphate dehydrogenase deficiency decrease the erythrocyte life span, an effect contributing to anemia. Most recently, erythro-cytes have been shown undergo apoptosis upon increase of cytosolic Ca2+ activity. The present study has performed explore whether enhance sensitivity erythrocytes osmotic shock, oxidative stress or energy depletion, all maneuvers known To this end, annexin binding indicator determined by FACS...

10.1159/000067907 article EN Cellular Physiology and Biochemistry 2002-01-01

Human erythrocytes express cation channels which contribute to the background leak of Ca2+, Na+ and K+. Excessive activation these upon energy depletion, osmotic shock, Cl- or oxidative stress triggers suicidal death (eryptosis), characterized by cell-shrinkage exposure phosphatidylserine at cell surface. Eryptotic cells are supposed be cleared from circulating blood. The present study aimed identify channels. RT-PCR revealed mRNA encoding non-selective channel TRPC6 in erythroid progenitor...

10.1159/000113760 article EN Cellular Physiology and Biochemistry 2008-01-01

Radiation is a highly efficient therapy in squamous head and neck carcinoma (HNSCC) treatment. However, local recurrence metastasis are common complications. Recent evidence shows that cancer-cell-derived exosomes modify tumour cell movement metastasis. In this study, we link radiation-induced changes of to their ability promote migration recipient HNSCC cells. We demonstrate isolated from irradiated donor cells boost the motility BHY FaDu. Molecular data identified enhanced AKT-signalling,...

10.1038/s41598-017-12403-6 article EN cc-by Scientific Reports 2017-09-25

Intraerythrocyte growth of the malaria parasite Plasmodium falciparum induces a Ca2+-permeable unselective cation conductance in host cell membrane which is inhibited by ethylisopropylamiloride (EIPA) and paralleled an exchange K+ Na+ cytosol. The present study has been performed to elucidate functional significance electrolyte exchange. Whole-cell patch-clamp experiments confirmed Ca2+ permeability EIPA sensitivity induced channel. In further experiments, ring stage-synchronized parasites...

10.1159/000075122 article EN Cellular Physiology and Biochemistry 2003-01-01

Background— Bartonella species are the only known bacterial pathogens causing vasculoproliferative disorders in humans (bacillary angiomatosis [BA]). Cellular and pathogenetic mechanisms underlying induction of BA largely unknown. Methods Results— Activation hypoxia-inducible factor-1 (HIF-1), key transcription factor involved angiogenesis, was detected henselae –infected host cells vitro by immunofluorescence, Western blotting, electrophoretic mobility shift, reporter gene assays...

10.1161/01.cir.0000155608.07691.b7 article EN Circulation 2005-02-22
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