Sökning: "fibril formation"
Visar resultat 1 - 5 av 94 avhandlingar innehållade orden fibril formation.
1. The Molecular Chaperone DNAJB6 - A Suppressor of Disease Related Amyloid Fibril Formation
Sammanfattning : Several neurodegenerative diseases are caused by peptides or proteins forming amyloid fibrils such as the Aβ peptide involved in Alzheimer’s disease and the huntingtin exon-1 with a prolonged polyglutamine (polyQ) stretch involved in Huntington’s disease. The ability to form amyloid fibrils is an intrinsic feature in all proteins. LÄS MER
2. Molecular mechanisms in amyloid fibril formation
Sammanfattning : This thesis concerns investigations on molecular processes and interactions that lead to amyloid fibril formation. Pulmonary surfactant protein C (SP-C), and a synthetic analogue thereof, SP-C(Leu), have similar properties in terms of charge distribution, hydrophobicity and secondary structure, yet they differ in their aggregation propensities. LÄS MER
3. Amyloid Fibril Formation - Dye Detection and Effects of Lipids
Sammanfattning : Amyloid fibrils are long fibrillar homopolymers of self-assembled proteins. They can be formed by essentially any polypeptide, but are of particular interest because of their occurrence in several incurable and debilitating human diseases, e.g. Alzheimer’s disease (AD). LÄS MER
4. Roles of intermolecular interactions in amyloid fibril formation mechanisms
Sammanfattning : Amyloid fibrils, a major pathological feature of several neurodegenerative disorders, are highly stable, insoluble aggregates of misfolded proteins. The formation of such aggregates involves a complex equilibrium between protein monomers, different on- and off-pathway transient oligomeric species, and amyloid fibrils. LÄS MER
5. Localized and systemic AL-amyloidosis : Aspects on protein structure, fibril formation and analytical methods
Sammanfattning : AL-amyloidosis is a protein storage disease and one of the most common types of amyloidosis. The precursor protein is a monoclonal immunoglobulin light chain which originates from plasma cell dyscrasia in systemic AL-amyloidosis and is probably produced by a local plasma cell clone in localized AL-amyloidosis. LÄS MER