Markus Bender

ORCID: 0000-0002-2381-116X
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About
Contact & Profiles
Research Areas
  • Platelet Disorders and Treatments
  • Blood properties and coagulation
  • Cell Adhesion Molecules Research
  • Antiplatelet Therapy and Cardiovascular Diseases
  • Blood groups and transfusion
  • Phosphodiesterase function and regulation
  • Venous Thromboembolism Diagnosis and Management
  • Complement system in diseases
  • Heparin-Induced Thrombocytopenia and Thrombosis
  • Blood Coagulation and Thrombosis Mechanisms
  • Pancreatic function and diabetes
  • Ion Channels and Receptors
  • Protein Kinase Regulation and GTPase Signaling
  • Cellular Mechanics and Interactions
  • Circadian rhythm and melatonin
  • Renal Diseases and Glomerulopathies
  • Doping in Sports
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Photoreceptor and optogenetics research
  • Amino Acid Enzymes and Metabolism
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Cellular transport and secretion
  • Peptidase Inhibition and Analysis
  • Erythrocyte Function and Pathophysiology
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms

Universitätsklinikum Würzburg
2012-2024

University of Würzburg
2013-2022

Institute for Biomedicine
2021

Centre Virchow-Villermé
2019

Brigham and Women's Hospital
2014-2015

Harvard University
2014-2015

Center for Translational Molecular Medicine
2014

Mass General Brigham
2013

University of Birmingham
2013

Deutsche Forschungsgemeinschaft
2007-2010

Platelet activation and aggregation are essential to limit posttraumatic blood loss at sites of vascular injury but also contributes arterial thrombosis, leading myocardial infarction stroke. Agonist-induced elevation [Ca2+]i is a central step in platelet activation, the underlying mechanisms not fully understood. A major pathway for Ca2+ entry nonexcitable cells involves receptor-mediated release intracellular stores, followed by store-operated calcium (SOC) channels plasma membrane....

10.1084/jem.20080302 article EN The Journal of Experimental Medicine 2008-06-16

The GlyT1 transporter has emerged as a key novel target for the treatment of schizophrenia. Herein, we report on optimization 2-alkoxy-5-methylsulfonebenzoylpiperazine class inhibitors to improve hERG channel selectivity and brain penetration. This effort culminated in discovery compound 10a (RG1678), first potent selective inhibitor have beneficial effect schizophrenic patients phase II clinical trial.

10.1021/jm100210p article EN Journal of Medicinal Chemistry 2010-05-21

Platelet inhibition is a major strategy to prevent acute ischemic cardiovascular and cerebrovascular events, which may, however, be associated with an increased bleeding risk. The (hem)immunoreceptor tyrosine activation motif-bearing platelet receptors, glycoprotein VI (GPVI) C-type lectin-like receptor 2 (CLEC-2), might promising antithrombotic targets because they can depleted from circulating platelets by antibody treatment, leading sustained protection, but only moderately times in...

10.1161/atvbaha.112.300672 article EN Arteriosclerosis Thrombosis and Vascular Biology 2013-03-01

Abstract Breakdown of vascular barriers is a major complication inflammatory diseases. Anucleate platelets form blood-clots during thrombosis, but also play crucial role in inflammation. While spatio-temporal dynamics clot formation are well characterized, the cell-biological mechanisms platelet recruitment to micro-environments remain incompletely understood. Here we identify Arp2/3-dependent lamellipodia as prominent morphological feature immune-responsive platelets. Platelets use scan for...

10.1038/s41467-020-19515-0 article EN cc-by Nature Communications 2020-11-13

MYH9 -related disease patients with mutations in the contractile protein nonmuscle myosin heavy chain IIA display, among others, macrothrombocytopenia and a mild-to-moderate bleeding tendency. In this study, we used three mouse lines, each one point mutation Myh9 gene at positions 702, 1424, or 1841, to investigate mechanisms underlying increased risk. Agonist-induced activation of mutant platelets was comparable controls. However, light phosphorylation after reduced platelets, which...

10.1126/sciadv.abn2627 article EN cc-by-nc Science Advances 2022-05-18

Platelets interact with multiple adhesion proteins during thrombogenesis, yet little is known about their ability to assemble fibronectin matrix. In vitro three-dimensional superresolution microscopy complemented by biophysical and biochemical methods revealed fundamental insights into how platelet contractility drives fibrillogenesis. adhering thrombus (fibronectin fibrin) versus basement membrane components (laminin collagen IV) pull fibrils along apical underneath basal membrane,...

10.1126/sciadv.abj8331 article EN cc-by-nc Science Advances 2022-03-11

Inherited or acquired disorders of platelet production and function can result in thrombocytopenia bleeding. Mouse models have proven useful for investigating the mechanisms that underlie these defects humans. Precise methods blood withdrawal, isolation measurement parameters are key generation reproducible conclusive data.Here, we provide three different protocols mouse to encourage research knowledge transfer between experienced laboratories, while at same time enabling less researchers...

10.1080/09537104.2018.1528345 article EN Platelets 2018-10-22
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