Excitotoxic inactivation of constitutive oxidative stress detoxification pathway in neurons can be rescued by PKD1
出版年份 2017 全文链接
标题
Excitotoxic inactivation of constitutive oxidative stress detoxification pathway in neurons can be rescued by PKD1
作者
关键词
-
出版物
Nature Communications
Volume 8, Issue 1, Pages -
出版商
Springer Nature
发表日期
2017-12-18
DOI
10.1038/s41467-017-02322-5
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- (2017) Federica Mastroiacovo et al. Molecular Brain
- Mutant KRas-Induced Mitochondrial Oxidative Stress in Acinar Cells Upregulates EGFR Signaling to Drive Formation of Pancreatic Precancerous Lesions
- (2016) Geou-Yarh Liou et al. Cell Reports
- PKD1 Protein Is Involved in Reactive Oxygen Species-mediated Mitochondrial Depolarization in Cooperation with Protein Kinase Cδ (PKCδ)
- (2015) Thianzhou Zhang et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Development of a neuroprotective peptide that preserves survival pathways by preventing Kidins220/ARMS calpain processing induced by excitotoxicity
- (2015) A Gamir-Morralla et al. Cell Death & Disease
- Role of DAPK in neuronal cell death
- (2013) Yuki Fujita et al. APOPTOSIS
- Neuroprotective Role of a Brain-Enriched Tyrosine Phosphatase, STEP, in Focal Cerebral Ischemia
- (2013) I. Deb et al. JOURNAL OF NEUROSCIENCE
- Dual specificity phosphatase 1 expression inversely correlates with NF-κB activity and expression in prostate cancer and promotes apoptosis through a p38 MAPK dependent mechanism
- (2013) Beatriz Gil-Araujo et al. Molecular Oncology
- Intravascular Perfusion of Carbon Black Ink Allows Reliable Visualization of Cerebral Vessels
- (2013) Mohammad R. Hasan et al. Jove-Journal of Visualized Experiments
- Kidins220 accumulates with tau in human Alzheimer's disease and related models: modulation of its calpain-processing by GSK3β/PP1 imbalance
- (2012) Celia López-Menéndez et al. HUMAN MOLECULAR GENETICS
- NF-κB Signaling Pathways
- (2012) Stefka Mincheva-Tasheva et al. NEUROSCIENTIST
- Protein kinase D1 (PKD1) activation mediates a compensatory protective response during early stages of oxidative stress-induced neuronal degeneration
- (2011) Arunkumar Asaithambi et al. Molecular Neurodegeneration
- Protein Kinase D Signaling: Multiple Biological Functions in Health and Disease
- (2011) Enrique Rozengurt PHYSIOLOGY
- The Role of Striatal-Enriched Protein Tyrosine Phosphatase (STEP) in Cognition
- (2011) Christopher James Fitzpatrick et al. Frontiers in Neuroanatomy
- High-Frequency Field Stimulation of Primary Neurons Enhances Ryanodine Receptor-Mediated Ca2+ Release and Generates Hydrogen Peroxide, Which Jointly Stimulate NF-κB Activity
- (2010) Denise Riquelme et al. ANTIOXIDANTS & REDOX SIGNALING
- DAPK1 Interaction with NMDA Receptor NR2B Subunits Mediates Brain Damage in Stroke
- (2010) Weihong Tu et al. CELL
- NR2B-NMDA receptor mediated modulation of the tyrosine phosphatase STEP regulates glutamate induced neuronal cell death
- (2010) Ranjana Poddar et al. JOURNAL OF NEUROCHEMISTRY
- A Novel Small-Molecule Inhibitor of Protein Kinase D Blocks Pancreatic Cancer Growth In vitro and In vivo
- (2010) K. B. Harikumar et al. MOLECULAR CANCER THERAPEUTICS
- Kidins220/ARMS downregulation by excitotoxic activation of NMDARs reveals its involvement in neuronal survival and death pathways
- (2009) C. Lopez-Menendez et al. JOURNAL OF CELL SCIENCE
- Requirement of protein kinase D1 for pathological cardiac remodeling
- (2008) J. Fielitz et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Dual-promoter lentiviral vectors for constitutive and regulated gene expression in neurons
- (2007) Sergio Gascón et al. JOURNAL OF NEUROSCIENCE METHODS
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