PINK1 deficiency sustains cell proliferation by reprogramming glucose metabolism through HIF1
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Title
PINK1 deficiency sustains cell proliferation by reprogramming glucose metabolism through HIF1
Authors
Keywords
-
Journal
Nature Communications
Volume 5, Issue 1, Pages -
Publisher
Springer Nature
Online
2014-07-24
DOI
10.1038/ncomms5514
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Note: Only part of the references are listed.- Loss of PINK1 Attenuates HIF-1 Induction by Preventing 4E-BP1-Dependent Switch in Protein Translation under Hypoxia
- (2014) W. Lin et al. JOURNAL OF NEUROSCIENCE
- Integrated analysis of microRNA and mRNA expression and association with HIF binding reveals the complexity of microRNA expression regulation under hypoxia
- (2014) Carme Camps et al. Molecular Cancer
- Enhancing nucleotide metabolism protects against mitochondrial dysfunction and neurodegeneration in a PINK1 model of Parkinson’s disease
- (2014) Roberta Tufi et al. NATURE CELL BIOLOGY
- HIF-1 mediates metabolic responses to intratumoral hypoxia and oncogenic mutations
- (2013) Gregg L. Semenza JOURNAL OF CLINICAL INVESTIGATION
- High-content genome-wide RNAi screens identify regulators of parkin upstream of mitophagy
- (2013) Samuel A. Hasson et al. NATURE
- A zebrafish model of PINK1 deficiency reveals key pathway dysfunction including HIF signaling
- (2013) M. Priyadarshini et al. NEUROBIOLOGY OF DISEASE
- Mitochondrial quality control turns out to be the principal suspect in parkin and PINK1-related autosomal recessive Parkinson's disease
- (2012) Olga Corti et al. CURRENT OPINION IN NEUROBIOLOGY
- Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences
- (2012) Nicole Exner et al. EMBO JOURNAL
- Endothelial Cell-Derived Nitric Oxide Enhances Aerobic Glycolysis in Astrocytes via HIF-1 -Mediated Target Gene Activation
- (2012) B. Brix et al. JOURNAL OF NEUROSCIENCE
- Time-Dependent Stabilization of Hypoxia Inducible Factor-1α by Different Intracellular Sources of Reactive Oxygen Species
- (2012) Maura Calvani et al. PLoS One
- γ-Glutamylcysteine detoxifies reactive oxygen species by acting as glutathione peroxidase-1 cofactor
- (2012) Ruben Quintana-Cabrera et al. Nature Communications
- Aerobic Glycolysis: Meeting the Metabolic Requirements of Cell Proliferation
- (2011) Sophia Y. Lunt et al. Annual Review of Cell and Developmental Biology
- Mitochondrial Quality Control and Dynamics in Parkinson's Disease
- (2011) Melissa K. McCoy et al. ANTIOXIDANTS & REDOX SIGNALING
- Hypoxia-inducible Factor-1 Activation in Nonhypoxic Conditions: The Essential Role of Mitochondrial-derived Reactive Oxygen Species
- (2010) David A. Patten et al. MOLECULAR BIOLOGY OF THE CELL
- Parkinson's disease mutations in PINK1 result in decreased Complex I activity and deficient synaptic function
- (2009) Vanessa A. Morais et al. EMBO Molecular Medicine
- Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission
- (2009) Ruben K. Dagda et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- PINK1-Associated Parkinson's Disease Is Caused by Neuronal Vulnerability to Calcium-Induced Cell Death
- (2009) Sonia Gandhi et al. MOLECULAR CELL
- The bioenergetic and antioxidant status of neurons is controlled by continuous degradation of a key glycolytic enzyme by APC/C–Cdh1
- (2009) Angel Herrero-Mendez et al. NATURE CELL BIOLOGY
- Silencing of PINK1 Expression Affects Mitochondrial DNA and Oxidative Phosphorylation in DOPAMINERGIC Cells
- (2009) Matthew E. Gegg et al. PLoS One
- Genomic variants at the PINK1 locus are associated with transcript abundance and plasma nonesterified fatty acid concentrations in European whites
- (2008) P. W. Franks et al. FASEB JOURNAL
- Clinical and molecular characterisation of a Parkinson family with a novel PINK1 mutation
- (2008) J. Prestel et al. JOURNAL OF NEUROLOGY
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