Caspase-3 activation via mitochondria is required for long-term depression and AMPA receptor internalization. - Wikidata - awgldk - TriplyDB

Caspase-3 activation via mitochondria is required for long-term depression and AMPA receptor internalization.

Caspase-3 activation via mitochondria is required for long-term depression and AMPA receptor internalization.

http://www.wikidata.org/entity/Q34019051

about

Caspases in synaptic plasticity Cell biology in neuroscience: Death of developing neurons: new insights and implications for connectivity Synapses and Alzheimer's disease Amyloid-β-Induced Dysregulation of AMPA Receptor Trafficking Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders Photoreceptor cell death and rescue in retinal detachment and degenerations Cell signaling and mitochondrial dynamics: Implications for neuronal function and neurodegenerative disease New roles for old enzymes: killer caspases as the engine of cell behavior changes Interactions between mitochondria and the transcription factor myocyte enhancer factor 2 (MEF2) regulate neuronal structural and functional plasticity and metaplasticity Serine racemase: a key player in apoptosis and necrosis The human epilepsy mutation GABRG2(Q390X) causes chronic subunit accumulation and neurodegeneration The core apoptotic executioner proteins CED-3 and CED-4 promote initiation of neuronal regeneration in Caenorhabditis elegans A Class of Allosteric Caspase Inhibitors Identified by High-Throughput Screening Old, new and emerging functions of caspases.Spines, plasticity, and cognition in Alzheimer's model mice Synaptopathies: synaptic dysfunction in neurological disorders - A review from students to students Chemical genetic identification of NDR1/2 kinase substrates AAK1 and Rabin8 Uncovers their roles in dendrite arborization and spine development Microtubule-associated protein tau is essential for long-term depression in the hippocampus Activity-dependent p25 generation regulates synaptic plasticity and Aβ-induced cognitive impairment FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration BRaf signaling principles unveiled by large-scale human mutation analysis with a rapid lentivirus-based gene replacement method.Caspase-3 activation as a bifurcation point between plasticity and cell death.Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice.Age-dependent regulation of synaptic connections by dopamine D2 receptors.Local caspase activation interacts with Slit-Robo signaling to restrict axonal arborization.Spatially selective photoconductive stimulation of live neurons.Long-term potentiation decay and memory loss are mediated by AMPAR endocytosis.Modeling the interactions of Alzheimer-related genes from the whole brain microarray data and diffusion tensor images of human brain.Protective role of 17β-estradiol on tumor necrosis factor-α-induced apoptosis in human nucleus pulposus cells The Role of Proteases in Hippocampal Synaptic Plasticity: Putting Together Small Pieces of a Complex Puzzle.Nerve growth factor-mediated inhibition of apoptosis post-caspase activation is due to removal of active caspase-3 in a lysosome-dependent manner.Damage of photoreceptor-derived cells in culture induced by light emitting diode-derived blue light NMDA receptor-dependent LTD is required for consolidation but not acquisition of fear memory.Caspase inhibition in select olfactory neurons restores innate attraction behavior in aged Drosophila.Dendritic mitoflash as a putative signal for stabilizing long-term synaptic plasticity.Cayman ataxia-related protein is a presynapse-specific caspase-3 substrate.Dietary and behavioral interventions protect against age related activation of caspase cascades in the canine brain.The intersection of amyloid beta and tau at synapses in Alzheimer's disease Mitochondria and neuroplasticity.Role of mitochondrial pathway in compression-induced apoptosis of nucleus pulposus cells.

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Caspase-3 activation via mitochondria is required for long-term depression and AMPA receptor internalization.

http://www.wikidata.org/entity/Q34019051

description

2010 nî lūn-bûn

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2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2010 թվականի մայիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年学术文章

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2010年学术文章

@zh-cn

2010年学术文章

@zh-hans

2010年学术文章

@zh-my

2010年学术文章

@zh-sg

2010年學術文章

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name

Caspase-3 activation via mitoc ...... AMPA receptor internalization.

@ast

Caspase-3 activation via mitoc ...... AMPA receptor internalization.

@en

Caspase-3 activation via mitoc ...... AMPA receptor internalization.

@nl

type

label

Caspase-3 activation via mitoc ...... AMPA receptor internalization.

@ast

Caspase-3 activation via mitoc ...... AMPA receptor internalization.

@en

Caspase-3 activation via mitoc ...... AMPA receptor internalization.

@nl

prefLabel

Caspase-3 activation via mitoc ...... AMPA receptor internalization.

@ast

Caspase-3 activation via mitoc ...... AMPA receptor internalization.

@en

Caspase-3 activation via mitoc ...... AMPA receptor internalization.

@nl

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Caspase-3 activation via mitoc ...... AMPA receptor internalization

@en

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Jie-Min Jia

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Jihoon Jo

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Morgan Sheng

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Shih-Ching Lo

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P2860

Structural basis of caspase-7 inhibition by XIAP

Structural basis for the inhibition of caspase-3 by XIAP

X-linked IAP is a direct inhibitor of cell-death proteases

The c-IAP-1 and c-IAP-2 proteins are direct inhibitors of specific caspases

IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases

Upstream regulatory role for XIAP in receptor-mediated apoptosis

NMR structure and mutagenesis of the third Bir domain of the inhibitor of apoptosis protein XIAP

Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD

LTP inhibits LTD in the hippocampus via regulation of GSK3beta

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Daniel J. Whitcomb

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