about
Passenger deletions generate therapeutic vulnerabilities in cancerTelomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice.FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasisThe in vivo gene expression signature of oxidative stressSF2312 is a natural phosphonate inhibitor of enolaseTrends in oxidative aging theoriesDietary restriction but not rapamycin extends disease onset and survival of the H46R/H48Q mouse model of ALSMnSOD deficiency has a differential effect on disease progression in two different ALS mutant mouse modelsAbsence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophyComplex III releases superoxide to both sides of the inner mitochondrial membraneQ-cycle bypass reactions at the Qo site of the cytochrome bc1 (and related) complexes.High rates of superoxide production in skeletal-muscle mitochondria respiring on both complex I- and complex II-linked substrates.Telomere dysfunction induces metabolic and mitochondrial compromise.Increased superoxide in vivo accelerates age-associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degenerationThe nature and mechanism of superoxide production by the electron transport chain: Its relevance to aging.Collateral Lethality: A new therapeutic strategy in oncologyENOblock Does Not Inhibit the Activity of the Glycolytic Enzyme EnolaseGenomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancerWhole-genome and multisector exome sequencing of primary and post-treatment glioblastoma reveals patterns of tumor evolutionOncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function.Dietary restriction attenuates age-associated muscle atrophy by lowering oxidative stress in mice even in complete absence of CuZnSOD.H(2)S-induced ectothermy: relevance to aging.Functional regulation of FoxO1 in neural stem cell differentiationConditional knockout of Mn-SOD targeted to type IIB skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity.Mitochondrial 'flashes': a radical concept repHined.HSP90 inhibition enhances cancer immunotherapy by upregulating interferon response genesThe 'mitoflash' probe cpYFP does not respond to superoxide.Multiple Q-cycle bypass reactions at the Qo site of the cytochrome bc1 complex.Architecture of the Qo site of the cytochrome bc1 complex probed by superoxide production.Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment.GAPDH is conformationally and functionally altered in association with oxidative stress in mouse models of amyotrophic lateral sclerosis.Deleterious action of FA metabolites on ATP synthesis: possible link between lipotoxicity, mitochondrial dysfunction, and insulin resistance.Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer.FOXO protects against age-progressive axonal degeneration.The Effect of Topoisomerase I Inhibitors on the Efficacy of T-Cell-Based Cancer Immunotherapy.Erratum: Corrigendum: Passenger deletions generate therapeutic vulnerabilities in cancerDenervation-induced skeletal muscle atrophy is associated with increased mitochondrial ROS productionAlterations in mitochondrial function, hydrogen peroxide release and oxidative damage in mouse hind-limb skeletal muscle during agingA critical evaluation of cpYFP as a probe for superoxideMutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer
P50
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P50
description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Florian Muller
@ast
Florian Muller
@en
Florian Muller
@es
Florian Muller
@nl
Florian Muller
@sl
type
label
Florian Muller
@ast
Florian Muller
@en
Florian Muller
@es
Florian Muller
@nl
Florian Muller
@sl
prefLabel
Florian Muller
@ast
Florian Muller
@en
Florian Muller
@es
Florian Muller
@nl
Florian Muller
@sl
P106
P21
P31
P496
0000-0001-7568-2948