Search results for "Beta protein"
showing 3 items of 3 documents
Full length cDNA of rat RT1.DMa and RT1.DMb and expression of RT1.DM genes in dendritic and Langerhans cells.
1997
MHC encoded DM heterodimers and classical MHC class II complexes meet in an endosomal/lysosomal compartment where DM heterodimers support peptide loading of MHC class II. Studies on peptide loading of rat class II and on peptide persistence in cells of the dendritic lineage prompted us to establish full length cDNA clones coding for the subunits alpha and beta of rat DM molecules as well as a mAb directed against the luminal moiety of the beta subunit. Here we describe the establishment of the first full length cDNA clones of rat RT1.DMa and RT1.DMb. The mode of expression of RT1.DM at the transcript level in bone marrow culture-derived dendritic cells, in Langerhans cells and in a number o…
From Small Peptides to Large Proteins against Alzheimer'sDisease.
2022
Alzheimer’s disease (AD) is the most common neurodegenerative disorder in the elderly. The two cardinal neuropathological hallmarks of AD are the senile plaques, which are extracellular deposits mainly constituted by beta-amyloids, and neurofibrillary tangles formed by abnormally phosphorylated Tau (p-Tau) located in the cytoplasm of neurons. Although the research has made relevant progress in the management of the disease, the treatment is still lacking. Only symptomatic medications exist for the disease, and, in the meantime, laboratories worldwide are investigating disease-modifying treatments for AD. In the present review, results centered on the use of peptides of different sizes invol…
The search for novel avenues for the therapy and prevention of Alzheimer's disease.
2006
The prevention and therapy of neurodegenerative disorders in the elderly is one of the greatest challenges facing molecular medicine today. Alzheimer's is an excellent example of a disease being studied by many groups worldwide. Indeed, while many molecular details of this disorder have been elucidated in the last two decades, there are still no strictly causal therapies available. While certain symptomatic pharmacological treatments are frequently employed, current molecular medicine research is focused on central Alzheimer-associated biochemical changes to find the key switch that turns the detrimental Alzheimer process on. Although amyloid beta proteins and tau proteins are the focus of …