KRANG · Kainate receptors and neuronal growth
6РП — Действия „Мария Кюри“
- Период
- 2006-05-04 → 2008-05-03
- Финансиране от ЕС
- 161 314 €
- Участници
- 1
- Схема
- IIF
Линиите свързват координатора с партньорите.
Накратко на български
Каинатовите рецептори и тяхната модификация се анализират при мозъчен удар, за да се разбере как се променят протеините в мозъка. Това помага за изясняване на механизмите, които водят до смърт на невроните при липса на кислород и глюкоза.
Кратко обяснение, генерирано от езиков модел по текста на CORDIS. Оригиналът е по-долу.
Резултати накратко
Final Activity Report Summary - KRANG (Kainate receptors and neuronal growth)
Cerebral ischaemia (stroke) is an extreme form of metabolic stress resulting from oxygen and glucose deprivation that most commonly occurs when the blood supply to a part of the brain is suddenly interrupted by occlusion of a vessel. Stroke is the third leading cause of death after coronary heart disease and cancer in the industrialised part of the world, and is also the single most common cause of severe disability. It is well established that brain ischaemia can cause neuronal death via different signalling cascades. The relative importance and interrelationships between these pathways; however, remain poorly understood. Excitatory ionotropic glutamate receptors (GluRs) have been long time considered as potential targets for antiischaemic drugs. GluRs are integral membrane proteins that mediate the majority of excitatory neurotransmission in the brain. In particular, the kainate type of GluR appears to provide a tractable target for therapeutic intervention. In this project we undertook a study to investigate the role of kainate receptors and the posttranslational modification in ischaemia using both in vivo and in vitro model systems. We have shown that SUMOylation can regulate kainate receptor (KAR) function. Here we investigated changes in protein SUMOylation and levels of KAR and AMPA receptor subunits and demonstrate that posttranslational modification by SUMO and down-regulation of AMPARs and KARs may play important roles in the pathophysiological response to ischemia.
Текст от CORDIS, на английски · Данни: CORDIS, © Европейски съюз
Цел на проекта
This project sets out to employ emergent techniques and state-of-the-art technology to investigate the cellular and molecular mechanisms underlying the trafficking and synaptic expression of the kainate receptor subunit GluR6 in developing hippocampal newer ones. Briefly, a series of chimeras of KAR subunits and new fluorophores including pH-sensitive GFP (pHluorin) and photoactivatable-GFP will be constructed, expressed in neurones by viral infection protocols and imaged using confocal microscopy to determine how kainate receptors behave in living hippocampal neurones and what pathways are involved in their trafficking. This questions are important because kainate receptors in general, and GluR6 in particular, have been implicated in neuronal development an d synapse stabilisation. Therefore, increased understanding of the processes that regulate these subunits will inform work on normal neuronal development and plasticity as well neuropathology associated with certain neurodegenerative conditions such as Al zheimer's disease.
Оригинален текст от CORDIS (на английски).
Участници
- UNIVERSITY OF BRISTOL · BRISTOL, CLIFTONКоординаторОбединеното кралство
Връзки
Данни: CORDIS, © Европейски съюз