Michael Bäder

ORCID: 0000-0003-4780-4164
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About
Contact & Profiles
Research Areas
  • Renin-Angiotensin System Studies
  • Receptor Mechanisms and Signaling
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Hormonal Regulation and Hypertension
  • Cellular transport and secretion
  • Parallel Computing and Optimization Techniques
  • Neuropeptides and Animal Physiology
  • Apelin-related biomedical research
  • Neurotransmitter Receptor Influence on Behavior
  • Distributed and Parallel Computing Systems
  • Mast cells and histamine
  • Pluripotent Stem Cells Research
  • Neuroendocrine regulation and behavior
  • Lipid Membrane Structure and Behavior
  • Adenosine and Purinergic Signaling
  • Advanced Numerical Methods in Computational Mathematics
  • Adipose Tissue and Metabolism
  • Blood Coagulation and Thrombosis Mechanisms
  • Seismic Imaging and Inversion Techniques
  • Animal Genetics and Reproduction
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Birth, Development, and Health
  • Neuroscience and Neuropharmacology Research
  • CRISPR and Genetic Engineering
  • RNA Research and Splicing

Max Delbrück Center
2016-2025

German Centre for Cardiovascular Research
2016-2025

Charité - Universitätsmedizin Berlin
2016-2025

University of Lübeck
2016-2025

Institute for Medical Biology
2025

Freie Universität Berlin
2002-2024

Humboldt-Universität zu Berlin
1998-2024

Technical University of Munich
2015-2024

Graz University of Technology
2012-2024

Universidade Federal de Minas Gerais
2009-2023

The renin–angiotensin system plays a critical role in blood pressure control and body fluid electrolyte homeostasis. Besides angiotensin (Ang) II, other Ang peptides, such as III [Ang-(2–8)], IV [Ang-(3–8)], Ang-(1–7) may also have important biological activities. has become an of interest the past few years, because its cardiovascular baroreflex actions counteract those II. Unique angiotensin-binding sites specific for this heptapeptide studies with selective antagonist indicated existence...

10.1073/pnas.1432869100 article EN Proceedings of the National Academy of Sciences 2003-06-26

The neurotransmitter serotonin [5-hydroxytryptamine (5-HT)] is causally involved in multiple central nervous facets of mood control and regulating sleep, anxiety, alcoholism, drug abuse, food intake, sexual behavior ([1][1]). In peripheral tissues, 5-HT regulates vascular tone, gut motility,

10.1126/science.1078197 article EN Science 2003-01-02

The liver can regenerate its volume after major tissue loss. In a mouse model of regeneration, thrombocytopenia, or impaired platelet activity resulted in the failure to initiate cellular proliferation liver. Platelets are carriers serotonin blood. thrombocytopenic mice, agonist reconstituted proliferation. expression 5-HT2A and 2B subtype receptors increased hepatectomy. Antagonists inhibited regeneration. Liver regeneration was also blunted mice lacking tryptophan hydroxylase 1, which is...

10.1126/science.1123842 article EN Science 2006-04-06

10.1016/s0006-2952(03)00556-2 article EN Biochemical Pharmacology 2003-09-16

The renin-angiotensin-aldosterone system has been causally implicated in obesity-associated hypertension. We studied the influence of obesity and weight reduction on circulating adipose tissue menopausal women. Blood samples were analyzed for angiotensinogen, renin, aldosterone, angiotensin-converting enzyme activity, angiotensin II. In biopsy samples, we renin-receptor, enzyme, II type-1 receptor gene expression. Obese women (n=19) had higher than lean (n=19), lower angiotensinogen...

10.1161/01.hyp.0000154361.47683.d3 article EN Hypertension 2005-01-04

Cardiomyocytes differentiated in vitro from pluripotent embryonic stem (ES) cells of line D3 via embryo-like aggregates (embryoid bodies) were characterized by the whole-cell patch-clamp technique during entire differentiation period. Spontaneously contracting cardiomyocytes enzymatically isolated collagenase embryoid body outgrowths early, intermediate, and terminal stages. The early exhibited an outwardly rectifying, transient K+ current sensitive to 4-aminopyridine inward Ca2+ but no Na+...

10.1161/01.res.75.2.233 article EN Circulation Research 1994-08-01

While serotonin (5-HT) co-localization with insulin in granules of pancreatic β-cells was demonstrated more than three decades ago, its physiological role the etiology diabetes is still unclear. We combined biochemical and electrophysiological analyses mice selectively deficient peripheral tryptophan hydroxylase (Tph1−/−) 5-HT to show that intracellular regulates secretion. found these are diabetic have an impaired secretion due lack pancreas. The pharmacological restoration levels rescued...

10.1371/journal.pbio.1000229 article EN cc-by PLoS Biology 2009-10-26

The renin-angiotensin system (RAS) is a key regulator of the cardiovascular system, electrolyte, and water balance. Here, we report identification characterization alamandine, new heptapeptide generated by catalytic action angiotensin-converting enzyme-2 angiotensin A or directly from angiotensin-(1-7).To characterize novel component RAS, alamandine.Using mass spectrometry observed that alamandine circulates in human blood can be formed angiotensin-(1-7) heart. Alamandine produces several...

10.1161/circresaha.113.301077 article EN Circulation Research 2013-02-28

Serotonin synthesis in mammals is initiated by 2 distinct tryptophan hydroxylases (TPH), TPH1 and TPH2. By genetically ablating TPH2, we created mice ( Tph2 −/− ) that lack serotonin the central nervous system. Surprisingly, these can be born survive until adulthood. However, depletion of signaling brain leads to growth retardation 50% lethality first 4 weeks postnatal life. Telemetric monitoring revealed more extended daytime sleep, suppressed respiration, altered body temperature control,...

10.1073/pnas.0810793106 article EN Proceedings of the National Academy of Sciences 2009-06-12

Serotonin is a major neurotransmitter in the central nervous system (CNS). Dysregulation of serotonin transmission CNS reported to be related different psychiatric disorders humans including depression, impulsive aggression and anxiety disorders. The most frequently prescribed antidepressants anxiolytics target serotonergic system. However, these drugs are not effective 20–30% cases. causes this failure as well molecular mechanisms involved origin psychological poorly understood....

10.1038/tp.2012.44 article EN cc-by Translational Psychiatry 2012-05-29

Influenza A viruses are a threat to humans due their ability cross species barriers, as illustrated by the 2009 H1N1v pandemic and sporadic H5N1 transmissions. Interspecies transmission requires adaptation of viral polymerase importin-α, cellular protein that mediates transport into nucleus where transcription replication genome takes place. In this study, we analysed replication, host specificity pathogenicity avian mammalian influenza viruses, in importin-α-silenced cells...

10.1038/ncomms1158 article EN cc-by-nc-nd Nature Communications 2011-01-18

Voluntary wheel running has long been known to induce precursor cell proliferation in adult hippocampal neurogenesis rodents. However, mechanisms that couple activity with the promitotic effect are not yet fully understood. Using tryptophan hydroxylase (TPH) 2 deficient ( Tph2 -deficient) mice lack brain serotonin, we explored relationship between serotonin signaling and exercise-induced neurogenesis. Surprisingly, -deficient exhibit normal baseline but impaired activity-induced...

10.1523/jneurosci.5855-12.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-05-08

The Ang II (Angiotensin II)-Angiotensin-(1-7) axis of the Renin Angiotensin System encompasses 3 enzymes that form Angiotensin-(1-7) [Ang-(1-7)] directly from II: ACE2 (angiotensin-converting enzyme 2), PRCP (prolylcarboxypeptidase), and POP (prolyloligopeptidase). We investigated their relative contribution to Ang-(1-7) formation in vivo also ex serum, lungs, kidneys using models genetic ablation coupled with pharmacological inhibitors. In wild-type (WT) mice, infusion resulted a rapid...

10.1161/hypertensionaha.119.14071 article EN Hypertension 2019-12-02
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