Search for dissertations about: "Munc18 Proteins"
Found 5 swedish dissertations containing the words Munc18 Proteins.
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1. Role of syntaxin-11 and munc18-2 in lymphocyte cytotoxic granule exocytosis
Abstract : Mutations in genes required for the exocytosis of cytotoxic granules by NK cells and cytotoxic T lymphocytes are associated with early-onset familial hemophagocytic lymphohistiocytosis (FHL). In this project, we examined how certain missense mutations in genes encoding syntaxin-11 and Munc18-2 abolish exocytosis and cause disease. READ MORE
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2. SNAP-25 and Cdk5 as exocytotic regulators : consequences for synaptic function and insulin release
Abstract : The process by which cells release substances through fusion of vesicles with the plasma membrane is called exocytosis. Regulated exocytosis needs to be tightly controlled in order to respond to the large variation in stimuli and demands for release of neurotransmitters, peptides and hormones. READ MORE
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3. Components controlling vesicle trafficking and regulated exocytosis in pancreatic beta-cells
Abstract : Regulated exocytosis is a sophisticated, well-organized and conserved multistage process underlying release of both neurotransmitters and hormones. Exocytosis is mediated by SNARE proteins that act at the center stage by forming a SNARE complex with the intrinsic capability to execute membrane fusion. READ MORE
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4. Molecular mechanisms of biphasic insulin secretion
Abstract : Pancreatic beta-cells secrete insulin in response to increase in blood glucose concentration with a rapid first phase and slower, sustained second phase. This secretion pattern is similar in entire pancreas, isolated islets of Langerhans and single beta-cells and it is disrupted in type 2-diabetes. READ MORE
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5. Studies of SNAP-25 in regulated membrane fusion : metabolic consequences and tuning of intracellular Ca(2+) dynamics in beta cells
Abstract : Increased release of insulin is usually regarded as a symptom of metabolic syndrome, contributing to insulin resistance in peripheral organs thus affecting glucose and insulin homeostasis. The existing animal models to address the metabolic syndrome are currently not optimal. READ MORE