N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death - Wikidata - awgldk - TriplyDB

N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death

N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death

http://www.wikidata.org/entity/Q37390204

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A new view of the lethal apoptotic pore The functional differences between pro-survival and pro-apoptotic B cell lymphoma 2 (Bcl-2) proteins depend on structural differences in their Bcl-2 homology 3 (BH3) domains.Enriched endogenous omega-3 fatty acids in mice protect against global ischemia injury.Reactive astrocytes function as phagocytes after brain ischemia via ABCA1-mediated pathway.Multiple functions of BCL-2 family proteins.The mitochondrial complex V-associated large-conductance inner membrane current is regulated by cyclosporine and dexpramipexole Bcl-xL is necessary for neurite outgrowth in hippocampal neurons In vivo CaspaseTracker biosensor system for detecting anastasis and non-apoptotic caspase activity.The gene silencing transcription factor REST represses miR-132 expression in hippocampal neurons destined to die Cell death in genome evolution Evolution of Bcl-2 homology motifs: homology versus homoplasy.Functions of BCL-X L at the Interface between Cell Death and Metabolism PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling.PINK1 protects against cell death induced by mitochondrial depolarization, by phosphorylating Bcl-xL and impairing its pro-apoptotic cleavage Mimicking Cdk2 phosphorylation of Bcl-xL at Ser73 results in caspase activation and Bcl-xL cleavage.New Perspectives on Genomic Imprinting, an Essential and Multifaceted Mode of Epigenetic Control in the Developing and Adult Brain.In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila.Casein kinase 1 suppresses activation of REST in insulted hippocampal neurons and halts ischemia-induced neuronal death.Contributions of Bcl-xL to acute and long term changes in bioenergetics during neuronal plasticity.Mitochondrial channels: ion fluxes and more.Bcl-xL in neuroprotection and plasticity.The mystery of BCL2 family: Bcl-2 proteins and apoptosis: an update.Connecting mitochondrial dynamics and life-or-death events via Bcl-2 family proteins.Promotion of Caspase Activation by Caspase-9-mediated Feedback Amplification of Mitochondrial Damage.The N-terminal helix of Bcl-xL targets mitochondria.Mesenchymal Stem Cell-Derived Extracellular Vesicles Ameliorates Hippocampal Synaptic Impairment after Transient Global Ischemia.Mouse Transient Global Ischemia Two-Vessel Occlusion Model.Inhibition of Bcl-xL prevents pro-death actions of ΔN-Bcl-xL at the mitochondrial inner membrane during glutamate excitotoxicity.Neuroprotection against permanent focal cerebral ischemia by ginkgolides A and B is associated with obstruction of the mitochondrial apoptotic pathway via inhibition of c-Jun N-terminal kinase in rats.Caudatin induces caspase-dependent apoptosis in human glioma cells with involvement of mitochondrial dysfunction and reactive oxygen species generation.ΔN-Bcl-xL, a therapeutic target for neuroprotection.One cell's poison is another cell's cure.Putative roles of mitochondrial Voltage-Dependent Anion Channel, Bcl-2 family proteins and c-Jun N-terminal Kinases in ischemic stroke associated apoptosis.

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N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death

http://www.wikidata.org/entity/Q37390204

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on 26 February 2012

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

@da

vědecký článek

@cs

name

N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death

@en

N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death.

@nl

type

label

N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death

@en

N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death.

@nl

prefLabel

N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death

@en

N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death.

@nl

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Nature Neuroscience

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N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death

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Brian A Roelofs

http://www.w3.org/2001/XMLSchema#string

Dimitry Ofengeim

http://www.w3.org/2001/XMLSchema#string

Elizabeth A Jonas

http://www.w3.org/2001/XMLSchema#string

Fabrizio Pontarelli

http://www.w3.org/2001/XMLSchema#string

Hongmei Li

http://www.w3.org/2001/XMLSchema#string

J Marie Hardwick

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John A Hickman

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Kambiz N Alavian

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R Suzanne Zukin

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Richard J Flannery

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P2860

Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors

Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis

Oligomeric Bax is a component of the putative cytochrome c release channel MAC, mitochondrial apoptosis-induced channel

Developmental shift of cyclophilin D contribution to hypoxic-ischemic brain injury

The c-Jun N-terminal protein kinase signaling pathway mediates Bax activation and subsequent neuronal apoptosis through interaction with Bim after transient focal cerebral ischemia

Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death

Ischemic insults derepress the gene silencer REST in neurons destined to die

The BCL-2 protein family: opposing activities that mediate cell death

An inhibitor of Bcl-2 family proteins induces regression of solid tumours

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

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574-580

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scholarly article

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10.1038/NN.3054

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4

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15

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2012-02-26T00:00:00Z

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221863066

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22366758

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3862259

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