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(gc11-2002)Biomolecular Simulation of Base Excision Repair and Protein Signaling


EMSL Project ID
2401

Abstract

Environmental factors including ionizing radiation contribute to continuous damage of cellular DNA, in addition to endogenous sources. The damage resulting from oxidative stress and ionizing radiation is primarily in the form of oxidized bases, single strand breaks, and loss of bases. These are the targets of the Base Excision Repair (BER) mechanism enzymes, including polymerase-? . Failure to correctly and timely repair these damaged DNA sites can result in cell death, carcinogenesis, or genetic diseases. Resulting mutations in cell signal transduction enzymes can lead to uncontrolled cell proliferation or differentiation. For example, mutations in Ras, the molecular switch in several growth-factor signaling pathways, have been found in about 30% of human tumors. These signaling pathways often involve a chain of protein kinases that activate or deactivate each other through phosphorylation reactions, eventually controlling the activation of transcription factors in the cell nucleus. This proposal seeks the massively parallel computing resources required to perform molecular modeling and simulation studies to enhance our understanding of the mechanism of human polymerase-? , one of the key enzymes in BER repair, and the cell signaling enzymes cyclic-AMP-dependent protein kinase and Ras. Specifically, this work will focus on the ?dynamics of DNA and damaged DNA ?dynamics and energetics of base flipping in DNA ?co-solvent effects on biomolecular structures, including DNA ?mechanism and fidelity of nucleotide insertion by BER enzyme human polymerase-? ?mechanism and inhibitor design for cyclic-AMP-dependent protein kinase ?dynamics and energetics of Ras and its complex with effector molecule Raf For the molecular dynamics simulations and electronic structure calculations, the proposed investigations will rely on NWChem, the massively parallel software for computational chemistry developed at EMSL. NWChem will also be used for the analysis of the generated molecular dynamics trajectories, and any additional analysis tools required for the proposed work will be developed within the analysis modules of NWChem.

Project Details

Project type
Capability Research
Start Date
2002-01-04
End Date
2005-01-06
Status
Closed

Team

Principal Investigator

T. Straatsma
Institution
Oak Ridge National Laboratory

Team Members

Banu Gopalan
Institution
Pacific Northwest National Laboratory

Matthew Ernst
Institution
Washington State University Tri-Cities

Maciej Haranczyk
Institution
Lawrence Berkeley National Laboratory

Wlodzimierz Apostoluk
Institution
University of Wroclaw

Seung Lee
Institution
Massachusetts Institute of Technology

Tomaso Frigato
Institution
Max Planck Institute of Biophysics

Alejandro Aceves-Gaona
Institution
Washington State University Tri-Cities

Wibke Sudholt
Institution
University of California, San Diego

C. F. Wong
Institution
University of California, San Diego

J Mccammon
Institution
University of California, San Diego

Erich Vorpagel
Institution
Environmental Molecular Sciences Laboratory

John Miller
Institution
Washington State University Tri-Cities

Robert Rittenhouse
Institution
Walla Walla University

Martin Zacharias
Institution
Technische Universität München

Paul Smith
Institution
Kansas State University

Related Publications

Barthel A, and M Zacharias. 2006. "Conformational Transitions in RNA Single Uridine and Adenosine Bulge Structures: A Molecular Dynamics Free Energy Simulation Study ." Biophysical Journal 90(7):2450-2462.
Minor groove deformability of DNA: A Molecular dynamics free energy simulation study