JNK3 perpetuates metabolic stress induced by Aβ peptides. - sprookjes - yvandenbroek - TriplyDB

JNK3 perpetuates metabolic stress induced by Aβ peptides.

JNK3 perpetuates metabolic stress induced by Aβ peptides.

http://www.wikidata.org/entity/Q36224075

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Current Research Therapeutic Strategies for Alzheimer's Disease Treatment c-Jun N-terminal Kinase (JNK) Signaling as a Therapeutic Target for Alzheimer's Disease Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease Stress kinases in the modulation of metabolism and energy balance Pro-Apoptotic Kinase Levels in Cerebrospinal Fluid as Potential Future Biomarkers in Alzheimer's Disease Palmitate Increases β-site AβPP-Cleavage Enzyme 1 Activity and Amyloid-β Genesis by Evoking Endoplasmic Reticulum Stress and Subsequent C/EBP Homologous Protein Activation.Insulin Resistance as a Link between Amyloid-Beta and Tau Pathologies in Alzheimer's Disease.Recent Insights into the Role of Unfolded Protein Response in ER Stress in Health and Disease.Endoplasmic reticulum stress mediates amyloid β neurotoxicity via mitochondrial cholesterol trafficking Design and synthesis of highly potent and isoform selective JNK3 inhibitors: SAR studies on aminopyrazole derivatives.A small molecule bidentate-binding dual inhibitor probe of the LRRK2 and JNK kinases.Structural basis and biological consequences for JNK2/3 isoform selective aminopyrazoles.Molecular and bioenergetic differences between cells with African versus European inherited mitochondrial DNA haplogroups: implications for population susceptibility to diseases.Soluble beta-amyloid peptides, but not insoluble fibrils, have specific effect on neuronal microRNA expression.EphrinB2 controls vessel pruning through STAT1-JNK3 signalling.Increased levels of cerebrospinal fluid JNK3 associated with amyloid pathology: links to cognitive decline.Serum- and Glucocorticoid-Inducible Kinase 1 Confers Protection in Cell-Based and in In Vivo Neurotoxin Models via the c-Jun N-Terminal Kinase Signaling Pathway.Amyloid-β precursor protein: Multiple fragments, numerous transport routes and mechanisms Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer's disease JNK pathway signaling: a novel and smarter therapeutic targets for various biological diseases.Small molecule LX2343 ameliorates cognitive deficits in AD model mice by targeting both amyloid β production and clearance.ABCA7 Deficiency Accelerates Amyloid-β Generation and Alzheimer's Neuronal Pathology.Mitochondrial biogenesis: a therapeutic target for neurodevelopmental disorders and neurodegenerative diseases The importance of tau phosphorylation for neurodegenerative diseases NGF controls APP cleavage by downregulating APP phosphorylation at Thr668: relevance for Alzheimer's disease.The CAMKK2-AMPK kinase pathway mediates the synaptotoxic effects of Aβ oligomers through Tau phosphorylation ER-stress in Alzheimer's disease: turning the scale?Evidence of Presynaptic Localization and Function of the c-Jun N-Terminal Kinase The unfolded protein response in Alzheimer's disease.Insulin resistance: an emerging link in Alzheimer's disease.Disturbance of endoplasmic reticulum proteostasis in neurodegenerative diseases.Involvement of 'stress-response' kinase pathways in Alzheimer's disease progression.Nuclear and cytosolic JNK signalling in neurons.Peptide mini-scaffold facilitates JNK3 activation in cells Pyridopyrimidinone Derivatives as Potent and Selective c-Jun N-Terminal Kinase (JNK) Inhibitors.Brain metabolic stress and neuroinflammation at the basis of cognitive impairment in Alzheimer's disease AMPK-mediated regulation of neuronal metabolism and function in brain diseases.Molecular mechanisms in the initiation phase of Wallerian degeneration.AMPK in Neurodegenerative Diseases.Modulation of AβPP and GSK3β by Endoplasmic Reticulum Stress and Involvement in Alzheimer's Disease.

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JNK3 perpetuates metabolic stress induced by Aβ peptides.

http://www.wikidata.org/entity/Q36224075

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name

JNK3 perpetuates metabolic stress induced by Aβ peptides.

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JNK3 perpetuates metabolic stress induced by Aβ peptides.

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JNK3 perpetuates metabolic stress induced by Aβ peptides.

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JNK3 perpetuates metabolic stress induced by Aβ peptides.

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JNK3 perpetuates metabolic stress induced by Aβ peptides.

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JNK3 perpetuates metabolic stress induced by Aβ peptides.

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J.NEURON.2012.06.024

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JNK3 perpetuates metabolic stress induced by Aβ peptides

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Ajaya J Kunwar

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Alan H Nagahara

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Chhavy Tep

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Dong Ju Park

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Hatice Gulcin Ozer

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Jae Cheon Ryu

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Kun Huang

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Kun Ping Lu

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Lucia Pastorino

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Mark H Tuszynski

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P2860

Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease

Complexes between the LKB1 tumor suppressor, STRAD alpha/beta and MO25 alpha/beta are upstream kinases in the AMP-activated protein kinase cascade

Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1

Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers

Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

Differential roles of JIP scaffold proteins in the modulation of amyloid precursor protein metabolism

The prolyl isomerase Pin1 regulates amyloid precursor protein processing and amyloid-beta production

AMPK phosphorylation of raptor mediates a metabolic checkpoint

Naturally secreted amyloid-beta increases mammalian target of rapamycin (mTOR) activity via a PRAS40-mediated mechanism

Human amyloid-beta synthesis and clearance rates as measured in cerebrospinal fluid in vivo

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10.1016/J.NEURON.2012.06.024

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Randy J. Nelson

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2012-09-01T00:00:00Z

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