Health Informatics And Implementation Science
Biostatistics And Health Services Research
Postdoctoral positions are available to study the relationship(s) between the Rb/E2F proliferation pathway and p53-dependent apoptosis. Areas of investigation include understanding why E2F1 is unique among the E2F family in its strong apoptosis signaling ability and determining the pathways that lead from E2F1 activation to cell death. Fellows will be associated with a highly motivated and interactive group of researchers studying aspects of cell cycle, apoptosis signaling and cancer using cell culture, virology and animal models. If interested, please contact: Timothy Kowalik Department of Molecular Genetics and Microbiology University of Massachusetts Medical School 55 Lake Avenue North Worcester, MA 01655 The University of Massachusetts Medical School is an Affirmative Action / Equal Opportunity Employer.
Rotation Projects Identify the region on E2F1 responsible for p53-mediated apoptosis. We know that a transcriptionally functional E2F1 is required for apoptosis signaling. We also know that E2F2 does not induce apoptosis in our system. Therefore, domains on E2F1 and E2F2 will be swapped to determine which E2F1 domain is responsible for apoptosis signaling. Role of nuclear kinases in E2F1 mediated apoptosis. Our recent efforts have revealed that E2F1 expression leads to the phosphorylation of p53 and this modification correlates with apoptosis. There are several candidate kinases that need to be analyzed for their contribution to p53 phosphorylation. A dominant negative approach will be used in this project to identify which kinase(s) contribute to the E2F1 signal to p53. Role of CMV IE proteins in proliferation. We have found that both IE1 and IE2 target different Rb family members. IE2 binds to Rb and IE1 interacts with p107. We now know that IE2 is a strong inducer of S phase but IE1 can only significantly modulate proliferation in cells lacking p53. We are interested in knowing why p53 can prevent IE1 from inducing S phase. Mechanism of p53 accumulation by CMV. It has recently been shown that CMV infection results in an accumulation of p53. We have recently found that IE1 expression also leads to p53 accumulation. We wish to determine the steps leading to p53 accumulation and the consequences of this event.
Focus: Cellular and organismal studies of viral infections
Barbara Helen Smith Chair in Preventive & Behavioral Medicine
Richard M. Haidack Professor in Medicine
Postdoctoral Research Fellow, Department of Biostatistics, University of Michigan 2016 Jan.- 2017 Nov. Mentor: Peter X.K. Song, Ph.D. Research in developing Bayesian Newton's Growth Models (NGMs) in the ELEMENT study. Collaboration with Dr. Bin Zhu. Research in developing statistical methods for estimating sleep duration from actigraphy data in the Early Life Exposures in Mexico to ENvironmental Toxicants (ELEMENT) study. Postdoctoral Research Fellow, Department of Epidemiology, University of Michigan 2015 Jan. -2015 Dec. Mentor: Lynda D. Lisabeth, Ph.D. Research in epidemiological data analyses in the Brain Attack Surveillance In Corpus Christi (BASIC) project. Research in developing statistical models to investigate built environment association with BMI in the Multi-Ethnic Study of Atherosclerosis (MESA). Collaboration with Dr. Brisa N. Sanchez. Research in Bayesian spatial modeling of a binary outcome with spatially varying coecients in neuro-imaging data. Collaboration with Dr. Timothy D. Johnson.
Population and Quantitative Health Sciences
Focus: Machine learning, digital epidemiology, mobile health and data visualization
Prevention Research Center at UMass Chan
Healthcare Delivery and Population Sciences at UMass Chan - Baystate
Joseph D. Early Chair in Biomedical Research