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Journal ArticleDOI

Immediate-early gene protein expression in neurons undergoing delayed death, but not necrosis, following hypoxic-ischaemic injury to the young rat brain

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TLDR
C-Jun showed a prolonged expression in neurons undergoing delayed, but not necrotic, cell death suggesting that they may be involved in the biochemical cascade that causes selective delayed neuronal death.
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This article is published in Molecular Brain Research.The article was published on 1994-08-01. It has received 192 citations till now. The article focuses on the topics: Brain-derived neurotrophic factor & Neurotrophic factors.

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Journal ArticleDOI

Ischemic Cell Death in Brain Neurons

TL;DR: A major unifying thread of the review is a consideration of how the changes occurring during and after ischemia conspire to produce damaging levels of free radicals and peroxynitrite to activate calpain and other Ca(2+)-driven processes that are damaging, and to initiate the apoptotic process.
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Inducible and constitutive transcription factors in the mammalian nervous system: control of gene expression by Jun, Fos and Krox, and CREB/ATF proteins

TL;DR: This article reviews findings up to the end of 1997 about the inducible transcription factors c-Jun, JunB, JunD, c-Fos, FosB, Fra,1, Fra-2, Krox-20 (Egr-2) and Krox -24 (NGFI-A, Egr-1, Zif268) as they pertain to gene expression in the mammalian nervous system and describes their expression and possible roles in glial cells.
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Activating Transcription Factor 3 (ATF3) Induction by Axotomy in Sensory and Motoneurons: A Novel Neuronal Marker of Nerve Injury

TL;DR: It is concluded that ATF3 is specifically induced in sensory and motoneurons in the spinal cord following nerve injury and should be regarded as an unique neuronal marker of nerve injury in the nervous system.
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Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death.

TL;DR: A GSH-depletion model of neurodegenerative disorders is provided, experimental verifications of this model are suggested, and potential therapeutic approaches for preventing or halting these diseases are proposed.
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Molecular targets in cerebral ischemia for developing novel therapeutics.

TL;DR: The current status on the molecular mechanisms of stroke pathophysiology is covered with an endeavour to identify potential molecular targets such as targeting postsynaptic density-95 (PSD-95)/N-methyl-d-aspartate (NMDA) receptor interaction, certain key proteins involved in oxidative stress, CaMKs and MAPKs (ERK, p38 and JNK) signalling, inflammation and cell death pathways.
References
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Journal ArticleDOI

Molecular cloning and expression of brain-derived neurotrophic factor.

TL;DR: The full primary structure of brain-derived neurotrophic factor is reported and it is established that these two neurotrophic factors are related both functionally and structurally.
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Cross-family dimerization of transcription factors Fos/Jun and ATF/CREB alters DNA binding specificity.

TL;DR: It is suggested that the Fos/Jun and ATF/CREB families of transcription factors, which function in coupling extracellular signals to alterations in expression of specific target genes, can be grouped into a superfamily of transcription factor.
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Inhibitors of protein synthesis and RNA synthesis prevent neuronal death caused by nerve growth factor deprivation.

TL;DR: The fact that sympathetic neurons must synthesize protein and RNA to die when deprived of NGF indicates that NGF, and presumably other neurotrophic factors, maintains neuronal survival by suppressing an endogenous, active death program.
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Continuous c-fos expression precedes programmed cell death in vivo

TL;DR: Evidence is provided showing that the continuous expression of Fos, beginning hours or days before the morphological demise of the cell, appears to be a hallmark of terminal differentiation and a harbinger of death.
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