Sökning: "Glycogen Synthase Kinase"

Visar resultat 1 - 5 av 18 avhandlingar innehållade orden Glycogen Synthase Kinase.

  1. 1. Beta-amyloid, tau-protein and cystatin C in the pathophysiology of Alzheimer´s disease

    Detta är en avhandling från Divison of Clinical Chemistry and Pharmacology, Lund University

    Författare :Maj-Linda Selenica; Lund University.; Lunds universitet.; [2005]
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Neurologi; neuropsykologi; neurofysiologi; neuropsychology; neurophysiology; Neurology; Medicine human and vertebrates ; Medicin människa och djur ; Clinical chemistry; Klinisk kemi; Kinase inhibitors; Tau protein; Cystatin C; Glycogen Synthase Kinase; Alzheimers Disease; Amyloid beta;

    Sammanfattning : 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. LÄS MER

  2. 2. Role of P70 S6 kinase in the formation of tau pathologies in Alzheimer´s disease

    Detta är en avhandling från Stockholm : Karolinska Institutet, Department of Clinical Neuroscience, Occupational Therapy and Elderly Care Research (NEUROTEC)

    Författare :Wen-Lin An; Karolinska Institutet.; Karolinska Institutet.; [2005]
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Alzheimer s disease; p70 S6 kinase; tau; protein translation; accumulation; phosphorylation;

    Sammanfattning : 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. LÄS MER

  3. 3. Regulation of carbohydrate metabolism in skeletal muscle during and after contraction

    Detta är en avhandling från Stockholm : Karolinska Institutet, Department of Physiology and Pharmacology

    Författare :Marie Sandström; Karolinska Institutet.; Karolinska Institutet.; [2006]
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Skeletal muscle; glucose transport; contraction; ROS; AMPK; glycogen phosphorylase; glycogen synthase;

    Sammanfattning : It is well known that exercise increases glucose transport into skeletal muscles. The regulation of this transport, however, is poorly understood. LÄS MER

  4. 4. In vitro modelling of tau phosphorylating kinases : emphasis of Cdk5

    Detta är en avhandling från Stockholm : Karolinska Institutet, Department of Neurobiology, Care Sciences and Society

    Författare :Anne Jämsä; Karolinska Institutet.; Karolinska Institutet.; [2007]
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES;

    Sammanfattning : 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. LÄS MER

  5. 5. Molecular consequences of cellular UDP-glucose deficiency

    Detta är en avhandling från Stockholm : Karolinska Institutet, Microbiology and Tumor Biology Center (MTC)

    Författare :Juan Carlos Higuita V; Karolinska Institutet.; Karolinska Institutet.; [2004]
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES;

    Sammanfattning : A Chinese hamster fibroblast mutant cell line, deficient in UDP-glucose (UDPG), denoted as Qc, and its counterpart cell line with normalized levels of UDPG (G3), were used to determine some molecular consequences of chronic UDPG deficiency. The UDPG deficient cells lacked glycogen, had elevated rates of glucose uptake and a decreased capacity to synthesize glycogen after 120h of culture. LÄS MER