Friday
Workshop Announcement:
The workshop goal is to bring together diverse perspectives of biophysical, computational and evolutionary scientists to understand the deleterious consequences of human disease mutations and the aggregation leading to neurodegenerative diseases. The study of amyloidogenesis and the structure of amyloid aggregates is leading to new theories and treatments, while the large amount of information on the human genome and other genomes has allowed computational and experimental approaches to comprehend why a given single nucleotide polymorphism may be deleterious and result in human disease. New computational approaches complement experimental results, making this workshop extremely timely. The workshop is designed to reach a very diverse audience consisting of roughly a 50:50 mix of experimentalists and computational scientists. There will be time for informal interactions.
This workshop is being sponsored jointly by DIMACS, the BioMAPS program, the Center for Molecular Biophysics and Biophysical Chemistry, and Robert Wood Johnson Medical School. DIMACS (The Center for Discrete Mathematics and Theoretical Computer Science at Rutgers) receives NSF support to develop and populate the interface between the mathematical-physical sciences and molecular biology, while the mission of the BioMAPS Institute is to promote research and education at the interface between the Biological, Mathematical, and Physical Sciences. The Center for Molecular Biophysics and Biophysical Chemistry at Rutgers provides a focus for scholarly activities at the interface of the biological and physical sciences at Rutgers and Robert Wood Johnson Medical School and coordinates a general academic program for graduate and undergraduate students.
Specific topics include
* Understanding the mechanism of protein association leading
to amyloidosis.
* Elucidation of the structure of the amyloid aggregates.
* Generation of native conformational states of proteins
from amino acid sequence.
* Computational analyses of the effects of mutations on
conformation and stability.
* Prediction of whether a SNP will be deleterious, leading
to human disease.
* Consideration of compensated pathogenic mutations and
their relation to disease.
* Prediction of disordered regions and the role of natively
unfolded regions in diseases.