Thomas Günther

ORCID: 0000-0003-3903-9490
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About
Contact & Profiles
Research Areas
  • Magnesium in Health and Disease
  • Epigenetics and DNA Methylation
  • Trace Elements in Health
  • Developmental Biology and Gene Regulation
  • Cancer-related gene regulation
  • Animal Genetics and Reproduction
  • Muscle Physiology and Disorders
  • Neonatal Respiratory Health Research
  • Bone Metabolism and Diseases
  • Blood disorders and treatments
  • Congenital heart defects research
  • Prostate Cancer Treatment and Research
  • Cystic Fibrosis Research Advances
  • Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
  • Human Health and Disease
  • Iron Metabolism and Disorders
  • Pluripotent Stem Cells Research
  • Noise Effects and Management
  • Heavy Metal Exposure and Toxicity
  • Hearing, Cochlea, Tinnitus, Genetics
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Adipose Tissue and Metabolism
  • Erythrocyte Function and Pathophysiology
  • interferon and immune responses
  • Protein Degradation and Inhibitors

Leibniz Institute of Virology (LIV)
2020

University of Freiburg
2002-2017

University Medical Center Freiburg
2006-2017

Center for Clinical Research (United States)
2012

Olgahospital
2010-2011

Freie Universität Berlin
1984-2009

Universitäts Frauenklinik
2005-2007

Baylor College of Medicine
2000

Institute of Bioinformatics and Systems Biology
1997-1998

Institute of Molecular Biology
1989-1997

Quinolones accumulate in cartilage, and because they form chelate complexes with divalent cations, possess the potential to induce a deficiency of functionally available magnesium. To test hypothesis that quinolone-induced arthropathy is caused (or aggravated) by magnesium we induced feeding juvenile rats magnesium-deficient diet for 9 days treated single oral doses ofloxacin (0, 100, 300, 600, or 1,200 mg/kg body weight) during this period. Additional groups on normal were correspondingly....

10.1128/aac.39.9.2013 article EN Antimicrobial Agents and Chemotherapy 1995-09-01

ABSTRACT We describe a new mouse mutation, designated open brain (opb), which results in severe defects the developing neural tube. Homozygous opb embryos exhibited an exen-cephalic malformation involving forebrain, midbrain and hindbrain regions. The primary defect of exen-cephaly could be traced back to failure initiate tube closure at midbrain-forebrain boundary. Severe malformations spinal cord dorsal root ganglia were observed thoracic region. mutant abnormal circular oval shape showed...

10.1242/dev.120.11.3119 article EN Development 1994-11-01

10.1016/0006-291x(85)90450-4 article EN Biochemical and Biophysical Research Communications 1985-07-01

10.1016/0006-291x(84)91627-9 article EN Biochemical and Biophysical Research Communications 1984-02-01

After skin wounding, the repair process is initiated by release of growth factors, cytokines, and bioactive lipids from injured vessels coagulated platelets. These signal molecules induce synthesis deposition a provisional extracellular matrix, as well fibroblast invasion into contraction wounded area. We previously showed that sphingosine-1-phosphate (S1P) triggers transduction cascade mediating nuclear translocation LIM-only protein Fhl2 in response to activation RhoA GTPase (Muller, J.M.,...

10.1083/jcb.200606043 article EN The Journal of Cell Biology 2007-04-09

The molecular pathophysiology of myeloproliferative neoplasms (MPNs) remains poorly understood. Based on the observation that transcription factor NF-E2 is often overexpressed in MPN patients, independent presence other aberrations, we generated mice expressing an transgene hematopoietic cells. These exhibit many features MPNs, including thrombocytosis, leukocytosis, Epo-independent colony formation, characteristic bone marrow histology, expansion stem and progenitor compartments,...

10.1084/jem.20110540 article EN cc-by-nc-sa The Journal of Experimental Medicine 2012-01-09

Abstract Coordination of energy metabolism is essential for homeostasis stem cells, whereas an imbalance in causes disease and accelerated aging. Here we show that deletion or enzymatic inactivation lysine-specific demethylase 1 (Lsd1) triggers senescence trophoblast cells (TSCs). Genome-wide transcriptional profiling TSCs following Lsd1 inhibition shows gene set enrichment aging metabolic pathways. Consistently, global metabolomic phenotypic analyses disclose unbalanced redox status,...

10.1038/cddis.2017.48 article EN cc-by Cell Death and Disease 2017-02-23

Deficiency of the lysosomal cysteine protease cathepsin L (Ctsl) in mice results a phenotype affecting multiple tissues, including thymus, epidermis, and hair follicles, heart develops as progressive dilated cardiomyopathy (DCM). To understand role Ctsl maintenance regular morphology function, it is critical to determine whether DCM Ctsl-/- primarily because lack expression activity cardiomyocytes or caused by additional extracardiac pathologies. Cardiomyocyte-specific mice, using an...

10.1074/jbc.m703447200 article EN cc-by Journal of Biological Chemistry 2007-10-18

Noise-induced hearing loss (NIHL) is significantly greater in rats fed a magnesium-deficient diet than on magnesium-rich diet. The was found to be negatively correlated with the magnesium concentration of perilymph. It suggested that also man, perilymph may importance determining susceptibility NIHL.

10.1121/1.389726 article EN The Journal of the Acoustical Society of America 1983-07-01

10.1016/0262-1746(86)90070-3 article EN Prostaglandins Leukotrienes and Medicine 1986-07-01
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