About: Peter H Willems

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researcher

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rdf:type	Item
description	forskare (sv) researcher (en) 연구원 (ko) ricercatore (it) 研究者 (ja) araştırmacı (tr) wetenschapper (nl) дослідник (uk) эрдэмтэн (mn) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy)
rdfs:label	Peter H Willems (en) Peter H Willems (es) Peter H Willems (nl) Peter H Willems (sl)
skos:prefLabel	Peter H Willems (en) Peter H Willems (es) Peter H Willems (nl) Peter H Willems (sl)
name	Peter H Willems (en) Peter H Willems (es) Peter H Willems (nl) Peter H Willems (sl)
given name	wds:Q55691930-D3D1F42E-1D9D-4CF7-AADF-01E92DE4B8F3
given name	Peter
instance of	wds:Q55691930-AB28C0D0-69A7-4246-8E8B-71FFAE9C9AAA
instance of	Homo sapiens
skos:altLabel	Peter H.G.M. Willems (en)
occupation	wds:Q55691930-169725D1-53E7-43C8-BA9D-CC487A27613E
sex or gender	wds:Q55691930-8D6885C5-DC27-4823-8788-1277D011D444
VIAF ID	wds:Q55691930-A2888A88-580A-4A94-87C8-BDD92C3A298B
GND ID	wds:Q55691930-edea517a-c246-45c6-887a-86069f65429a
family name	wds:Q55691930-E2E0F4B3-E552-404E-9453-7BBB584D019B
VIAF ID	http://viaf.org/viaf/3559149719109711130007
GND ID	https://d-nb.info/gnd/1133590942
occupation	researcher
sex or gender	male
VIAF ID	3559149719109711130007
GND ID	1133590942
family name	Willems
ORCID iD	wds:Q55691930-1FB68BDB-E583-4677-A13A-9FA46A862A8A
ORCID iD	https://orcid.org/0000-0002-0915-1599
ORCID iD	0000-0002-0915-1599
ResearcherID	wds:Q55691930-C2BAEE49-B58F-405C-BFA8-2D5DA97B7B37
ResearcherID	L-4759-2015
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q55691930
is author of	Acyl-CoA dehydrogenase 9 is required for the biogenesis of oxidative phosphorylation complex I Cytosolic signaling protein Ecsit also localizes to mitochondria where it interacts with chaperone NDUFAF1 and functions in complex I assembly Mutations in NDUFAF3 (C3ORF60), encoding an NDUFAF4 (C6ORF66)-interacting complex I assembly protein, cause fatal neonatal mitochondrial disease mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity. Identification of mitochondrial complex I assembly intermediates by tracing tagged NDUFS3 demonstrates the entry point of mitochondrial subunits NDUFA2 complex I mutation leads to Leigh disease Human mitochondrial complex I assembly is mediated by NDUFAF1. The coxsackievirus 2B protein increases efflux of ions from the endoplasmic reticulum and Golgi, thereby inhibiting protein trafficking through the Golgi Determinants for Membrane Association and Permeabilization of the Coxsackievirus 2B Protein and the Identification of the Golgi Complex as the Target Organelle The creatine kinase system is essential for optimal refill of the sarcoplasmic reticulum Ca2+ store in skeletal muscle. Targeting mitochondrial complex I using BAY 87-2243 reduces melanoma tumor growth. OXPHOS mutations and neurodegeneration Human NADH:ubiquinone oxidoreductase deficiency: radical changes in mitochondrial morphology? Mammalian mitochondrial complex I: biogenesis, regulation, and reactive oxygen species generation. Complex I disorders: causes, mechanisms, and development of treatment strategies at the cellular level. Mitoenergetic Dysfunction Triggers a Rapid Compensatory Increase in Steady-State Glucose Flux. Statin-Induced Myopathy Is Associated with Mitochondrial Complex III Inhibition. Mitochondrial dysfunction in primary human fibroblasts triggers an adaptive cell survival program that requires AMPK-α. Metabolic consequences of NDUFS4 gene deletion in immortalized mouse embryonic fibroblasts. Mitigation of NADH: ubiquinone oxidoreductase deficiency by chronic Trolox treatment. Trolox-sensitive reactive oxygen species regulate mitochondrial morphology, oxidative phosphorylation and cytosolic calcium handling in healthy cells. Quantifying small molecule phenotypic effects using mitochondrial morpho-functional fingerprinting and machine learning. Complex I and complex III inhibition specifically increase cytosolic hydrogen peroxide levels without inducing oxidative stress in HEK293 cells Mitochondrial hyperpolarization during chronic complex I inhibition is sustained by low activity of complex II, III, IV and V. A mutation in the FAM36A gene, the human ortholog of COX20, impairs cytochrome c oxidase assembly and is associated with ataxia and muscle hypotonia. Superoxide production is inversely related to complex I activity in inherited complex I deficiency. Mitochondrial and cytosolic thiol redox state are not detectably altered in isolated human NADH:ubiquinone oxidoreductase deficiency. Mitochondrial network complexity and pathological decrease in complex I activity are tightly correlated in isolated human complex I deficiency. A catalytic defect in mitochondrial respiratory chain complex I due to a mutation in NDUFS2 in a patient with Leigh syndrome Inhibition of complex I of the electron transport chain causes O2-. -mediated mitochondrial outgrowth. Coxsackievirus protein 2B modifies endoplasmic reticulum membrane and plasma membrane permeability and facilitates virus release. Reconstruction of the complete ouabain-binding pocket of Na,K-ATPase in gastric H,K-ATPase by substitution of only seven amino acids Ca2+-mobilizing agonists increase mitochondrial ATP production to accelerate cytosolic Ca2+ removal: aberrations in human complex I deficiency. Inhibition of mitochondrial Na+-Ca2+ exchange restores agonist-induced ATP production and Ca2+ handling in human complex I deficiency. Reduced cholecystokinin receptor phosphorylation and restored signalling in protein kinase C down-regulated rat pancreatic acinar cells. Functional expression of mutations in the human NaCl cotransporter: evidence for impaired routing mechanisms in Gitelman's syndrome Redox Homeostasis and Mitochondrial Dynamics. G37R SOD1 mutant alters mitochondrial complex I activity, Ca(2+) uptake and ATP production. Computer-assisted live cell analysis of mitochondrial membrane potential, morphology and calcium handling. Decreased intracellular ATP content and intact mitochondrial energy generating capacity in human cystinotic fibroblasts Mitochondrial Ca2+ homeostasis in human NADH:ubiquinone oxidoreductase deficiency. Mitochondrial complex I deficiency: from organelle dysfunction to clinical disease. Phytanic acid impairs mitochondrial respiration through protonophoric action. Contiguous gene deletion of ELOVL7, ERCC8 and NDUFAF2 in a patient with a fatal multisystem disorder Pharmacological targeting of mitochondrial complex I deficiency: the cellular level and beyond. Baculovirus complementation restores a novel NDUFAF2 mutation causing complex I deficiency. Native LDL potentiate TNF alpha and IL-8 production by human mononuclear cells. The diacylglycerol kinase inhibitor, R59022, potentiates cholecystokinin-induced enzyme secretion from rabbit pancreatic acini Phe783, Thr797, and Asp804 in transmembrane hairpin M5-M6 of Na+,K+-ATPase play a key role in ouabain binding. Inherited complex I deficiency is associated with faster protein diffusion in the matrix of moving mitochondria. Homomultimerization of the coxsackievirus 2B protein in living cells visualized by fluorescence resonance energy transfer microscopy Mitochondrial complex III stabilizes complex I in the absence of NDUFS4 to provide partial activity

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