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Selective Neuronal Vulnerability to Oxidative Stress in the Brain
In this review, the currently known molecular and cellular factors that contribute to SNV to OS are summarized and include high intrinsic OS, high demand for ROS/RNS-based signaling, low ATP production, mitochondrial dysfunction, and high inflammatory response in vulnerable neurons.
Molecular biology of glutamate receptors in the central nervous system and their role in excitotoxicity, oxidative stress and aging
- E. Michaelis
- Biology, ChemistryProgress in neurobiology
- 2 March 1998
Direct measurement of glutamate release in the brain using a dual enzyme-based electrochemical sensor
Anti-apoptotic protein Bcl-2 interacts with and destabilizes the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA).
- E. Dremina, V. Sharov, KESHAVA N. Kumar, A. Zaidi, E. Michaelis, C. Schöneich
- Biology, Computer ScienceBiochemical Journal
- 15 October 2004
The results suggest that the direct interaction of Bcl-2 with SERCA may be involved in the regulation of apoptotic processes in vivo through modulation of cytoplasmic and/or endoplasmic reticulum calcium levels required for the execution of apoptosis.
Bioenergetic flux, mitochondrial mass and mitochondrial morphology dynamics in AD and MCI cybrid cell lines.
Reduced bioenergetic function is present during very early AD, is not brain-limited and induces protean retrograde responses that likely have both adaptive and mal-adaptive consequences.
Oxidative inactivation of purified plasma membrane Ca2+-ATPase by hydrogen peroxide and protection by calmodulin.
- A. Zaidi, Lorena B. Barrón, V. Sharov, C. Schöneich, E. Michaelis, M. Michaelis
- Biology, ChemistryBiochemistry
- 21 October 2003
In the present studies, inhibition of PMCA by H( 2)O(2) was characterized in enzyme purified from human erythrocyte membranes, indicating a CaM-induced conformational state resistant to oxidation.
Transgenic Expression of Glud1 (Glutamate Dehydrogenase 1) in Neurons: In Vivo Model of Enhanced Glutamate Release, Altered Synaptic Plasticity, and Selective Neuronal Vulnerability
The Tg mice were significantly more resistant than wild-type mice to induction and duration of anesthesia produced by anesthetics that suppress Glu neurotransmission and might be a useful model for the effects of lifelong excess synaptic Glu release on CNS neurons and for age-associated neurodegenerative processes.
Cloning of cDNA for the glutamate-binding subunit of an NMDA receptor complex
The isolation and characterization of a protein complex of four major proteins that represents an intact complex of the NMDA receptor ion channel is reported and the cloning of the cDNA for one of the subunits of this receptor complex, the glutamate-binding protein is reported on.
Genomic and biochemical approaches in the discovery of mechanisms for selective neuronal vulnerability to oxidative stress
Low energy reserves and high intrinsic stress levels are two underlying factors for neuronal selective vulnerability to OS and these mechanisms can be targeted in the future for the protection of vulnerable neurons.