Peter H.G.M. Willems

ORCID: 0000-0002-0915-1599
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • ATP Synthase and ATPases Research
  • Metabolism and Genetic Disorders
  • Ion Transport and Channel Regulation
  • Pancreatic function and diabetes
  • Ion channel regulation and function
  • Protein Kinase Regulation and GTPase Signaling
  • Neuropeptides and Animal Physiology
  • Receptor Mechanisms and Signaling
  • Adipose Tissue and Metabolism
  • Neurobiology and Insect Physiology Research
  • Metabolism, Diabetes, and Cancer
  • Redox biology and oxidative stress
  • Electrolyte and hormonal disorders
  • Signaling Pathways in Disease
  • Advanced X-ray and CT Imaging
  • Viral Infections and Immunology Research
  • Cell Adhesion Molecules Research
  • Neuroscience and Neural Engineering
  • Cardiac electrophysiology and arrhythmias
  • Amino Acid Enzymes and Metabolism
  • Medical Imaging Techniques and Applications
  • RNA regulation and disease
  • Digital Radiography and Breast Imaging
  • Neuroendocrine regulation and behavior

Radboud University Nijmegen
2014-2023

Radboud University Medical Center
2014-2023

Radboud Institute for Molecular Life Sciences
2012-2023

Flemish Government
2023

University Medical Center
2002-2020

Netherlands Organisation for Applied Scientific Research
2019

Khondrion (Netherlands)
2015

Scientific Consulting Group
2015

Ghent University
2005

Imaging Center
2004

Epigenetic reprogramming of myeloid cells, also known as trained immunity, confers nonspecific protection from secondary infections. Using histone modification profiles human monocytes with the Candida albicans cell wall constituent β-glucan, together a genome-wide transcriptome, we identified induced expression genes involved in glucose metabolism. Trained display high consumption, lactate production, and ratio nicotinamide adenine dinucleotide (NAD(+)) to its reduced form (NADH),...

10.1126/science.1250684 article EN Science 2014-09-25

In mammals, the extracellular calcium concentration is maintained within a narrow range despite large variations in daily dietary input and body demand. The small intestine kidney constitute influx pathways into Ca2+ pool and, therefore, play primary role homeostasis. We identified an apical Ca2+influx channel, which expressed proximal intestine, distal part of nephron placenta. This novel epithelial channel (ECaC) 730 amino acids contains six putative membrane-spanning domains with...

10.1074/jbc.274.13.8375 article EN cc-by Journal of Biological Chemistry 1999-03-01

Inhibition of complex I (CI) the mitochondrial respiratory chain by BAY 87-2243 ('BAY') triggers death BRAFV600E melanoma cell lines and inhibits in vivo tumor growth. Here we studied mechanism which this inhibition induces death. treatment depolarized membrane potential (Δψ), increased cellular ROS levels, stimulated lipid peroxidation reduced glutathione levels. These effects were paralleled opening permeability transition pore (mPTP) stimulation autophagosome formation mitophagy....

10.1038/cddis.2017.133 article EN cc-by Cell Death and Disease 2017-03-30

There are marked mitochondrial abnormalities in parkin-knock-out Drosophila and other model systems. The aim of our study was to determine function morphology parkin-mutant patients. We also investigated whether pharmacological rescue impaired may be possible human tissue.

10.1002/ana.21492 article EN Annals of Neurology 2008-11-01

The recently cloned epithelial Ca<sup>2+</sup> channel (ECaC) constitutes the Ca<sup>2+</sup>influx pathway in 1,25-dihydroxyvitamin D<sub>3</sub>-responsive epithelia. We have combined patch-clamp analysis and fura-2 fluorescence microscopy to functionally characterize ECaC heterologously expressed HEK293 cells. intracellular concentration ECaC-expressing cells was closely correlated with applied electrochemical gradient, demonstrating distinctive permeability constitutive activation of...

10.1074/jbc.275.6.3963 article EN cc-by Journal of Biological Chemistry 2000-02-01

Recent evidence indicates that oxidative stress is central to the pathogenesis of a wide variety degenerative diseases, aging, and cancer. Oxidative occurs when delicate balance between production detoxification reactive oxygen species disturbed. Mammalian cells respond this condition in several ways, among which change mitochondrial morphology. In present study, we have used rotenone, an inhibitor complex I respiratory chain, thought increase O 2 − · production, mitoquinone (MitoQ),...

10.1152/ajpcell.00607.2004 article EN AJP Cell Physiology 2005-01-13

Abstract. The recently cloned epithelial Ca 2+ channel (ECaC), which is expressed primarily in 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 )-responsive -transporting epithelia, postulated to constitute the rate-limiting step active reabsorption. In present study, effect of 1,25(OH) was investigated on ECaC mRNA and protein levels kidneys rats that were raised a vitamin D—depleting diet. This diet decreased serum concentration significantly, accompanied by marked drop level. Both normalized within...

10.1681/asn.v1271342 article EN Journal of the American Society of Nephrology 2001-07-01

Abstract. The epithelial Ca 2+ channel (ECaC), which is exclusively expressed in 1,25-dihydroxyvitamin D 3 -responsive tissues, i.e. , kidney, intestine, and placenta, postulated to constitute the initial step process of transcellular transport. To strengthen this function, present study compares segmental cellular distribution ECaC other transport proteins known be involved In rabbit mRNA protein expression were primarily connecting tubule. Immunopositive staining for was found at apical...

10.1681/asn.v1171171 article EN Journal of the American Society of Nephrology 2000-07-01

Ecsit is a cytosolic adaptor protein essential for inflammatory response and embryonic development via the Toll-like BMP (bone morphogenetic protein) signal transduction pathways, respectively. Here, we demonstrate mitochondrial function (an evolutionary conserved signaling intermediate in Toll pathways) assembly of complex I (NADH:ubiquinone oxidoreductase). An N-terminal targeting directs to mitochondria, where it interacts with chaperone NDUFAF1 500- 850-kDa complexes as demonstrated by...

10.1101/gad.408407 article EN Genes & Development 2007-03-01

Complex I (NADH:ubiquinone oxidoreductase) is the largest multisubunit assembly of oxidative phosphorylation system, and its malfunction associated with a wide variety clinical syndromes ranging from highly progressive, often early lethal, encephalopathies to neurodegenerative disorders in adult life. The changes mitochondrial structure function that are at basis symptoms poorly understood. Video-rate confocal microscopy cells pulse-loaded mitochondria-specific rhodamine 123 followed by...

10.1152/ajpcell.00104.2005 article EN AJP Cell Physiology 2005-05-19

Loss-of-function mutations in the gene encoding mitochondrial PTEN-induced putative kinase 1 (PINK1) are a major cause of early-onset familial Parkinson's disease (PD). Recent studies have highlighted an important function for PINK1 clearing depolarized mitochondria by mitophagy. However, role and cellular functioning physiological conditions is still incompletely understood. Here, we investigate calcium (Ca2+) homeostasis PINK1-knockdown PINK1-knockout mouse cells, both basal metabolic...

10.1242/jcs.078303 article EN cc-by Journal of Cell Science 2011-03-09

Numerous studies have demonstrated that functional mitochondria are required for tumorigenesis, suggesting mitochondrial oxidative phosphorylation (OXPHOS) might be a potential target cancer therapy. In this study, we investigated the effects of BAY 87-2243, small molecule inhibits first OXPHOS enzyme (complex I), in melanoma vitro and vivo.BAY 87-2243 decreased oxygen consumption induced partial depolarization membrane potential. This was associated with increased reactive species (ROS)...

10.1186/s40170-015-0138-0 article EN cc-by Cancer & Metabolism 2015-10-07

Mitochondrial complex I (CI) is a multi-subunit enzyme that forms the major entry point of nicotinamide adenine dinucleotide (NADH) electrons into respiratory chain. Mutations in NDUFS4 gene, encoding an accessory subunit this complex, cause Leigh-like phenotype humans. To study nature and penetrance CI defect different tissues, we investigated role mice with fatal mitochondrial encephalomyopathy, caused by systemic inactivation Ndufs4 gene. We report absence mouse tissues results decreased...

10.1093/hmg/ddr446 article EN Human Molecular Genetics 2011-09-28
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