Search for dissertations about: "Glycogen Synthase Kinase"
Showing result 1 - 5 of 21 swedish dissertations containing the words Glycogen Synthase Kinase.
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1. Beta-amyloid, tau-protein and cystatin C in the pathophysiology of Alzheimer´s disease
Abstract : Alzheimer´s Disease (AD) is a progressive neurodegenerative dementia characterized by the extracellular accumulation of the beta-amyloid (Ab) peptide into plaques and intracellular phosphorylation and accumulation of tau protein into neurofibrillary tangles (NFT). Inflammation due to astrocytic and microglial activation is one of the ongoing processes in the disease giving rise to cytokine production and oxidative stress. READ MORE
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2. Role of p70 S6 kinase in the formation of tau pathologies in Alzheimer’s disease
Abstract : One of the important neuropathological features of Alzheimer's disease (AD) is the tau pathology seen as accumulation and hyperphosphorylation of this protein. Evidences showed that tau could be phosphorylated mostly at serine/threonine (S/T) residues by many kinases, including protein kinase B, glycogen synthase kinase (GSK)-3beta, extracellular signal-regulated kinase (ERK1/2), ERK1/2 kinase (MEK1/2), c-Jun Nterminal kinase (JNK), and p38. READ MORE
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3. Studies on exercise and glycogen re-synthesis in skeletal muscles of pigs with the PRKAG3 mutation
Abstract : AMP-activated protein kinase (AMPK) plays an important role in the regulation of glucose and lipid metabolism in skeletal muscle. Many pigs of Hampshire origin have a naturally occurring mutation situated in the PRKAG3 gene which encodes a muscle-specific isoform of the AMPK γ3-subunit. READ MORE
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4. Regulation of carbohydrate metabolism in skeletal muscle during and after contraction
Abstract : It is well known that exercise increases glucose transport into skeletal muscles. The regulation of this transport, however, is poorly understood. READ MORE
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5. In vitro modelling of tau phosphorylating kinases : emphasis of Cdk5
Abstract : The main hallmarks of Alzheimer’s disease (AD) are extracellular deposits of betaamyloid (Aβ) and intracellular neurofibrillary tangles (NFT) composed of highly phosphorylated tau protein. Abnormal hyperphosphorylation of tau is the most deleterious step in NFT formation making the use of kinase inhibitors an attractive treatment possibility in AD. READ MORE