Welcome to the Department of Biochemistry at Boston University School of Medicine. We are a highly interactive group of faculty, graduate students, and postdoctoral fellows with diverse research interests in biochemistry, cell biology, molecular biology, and genetics. We use cutting-edge technologies and experimental systems to address the cellular and molecular mechanisms of biological processes, particularly those that relate broadly to human disease.
Specific research themes within the department include Neuroscience & Aging; Signal Transduction & Cancer; ECM/Cellular Injury; Metabolism, Obesity/Diabetes; Proteomics, Glycomics & Lipidomics; and Development.
Our department offers a Master of Arts and a PhD with the option of a combined MD and PhD.
As part of the Division of Graduate Medical Sciences, we are committed to the education of graduate, medical, and dental students. The emphasis of our graduate program is on comprehensive research training in our faculty members’ laboratories. In addition, many of our nearly 50 graduate students join our active research labs through the Cell and Molecular Biology Program.
Under the direction of our Chair, Dr. David A. Harris, our department has embarked on an exciting, new expansion initiative, with the recruitment of new faculty members and substantial renovation of our research laboratories.
The Department of Biochemistry within Boston University School of Medicine is part of a large medical school/hospital complex that includes state-of-the-art laboratories, mass spectrometry resources, confocal laser scanning microscopy, and transgenic animal facilities.
Graduate training combines integrated coursework in biochemistry, cell biology, molecular biology, genetics, and genomics with extensive research training. We use cutting-edge technologies and experimental systems to address the cellular and molecular mechanisms of biological processes, particularly those that relate broadly to human disease. Students may take advantage of the full breadth of training in modern biochemistry offered in the department through their choice of elective courses, medical school-wide seminars, and research.
Students enjoy a highly interactive environment that provides excellent preparation for a variety of careers in the biomedical sciences. While many of our recent PhD graduates are pursuing careers in academia, an increasing number are now finding opportunities in other sectors.
Neuroscience & Aging
As our population ages, mainly due to advances in medical research, we are faced with greater numbers of individuals above the age of 65 and a plethora of age-related diseases. People above 65 years old have increased risk of developing disorders such as atherosclerosis, heart disease, diabetes, cancer, a list of neurodegenerative diseases including Alzheimer’s and Parkinson’s, as well as other conditions caused by the deposition of aggregated amyloid protein fibrils, collectively called amyloidoses. The Department of Biochemistry offers graduate students exciting opportunities to study age-related diseases in a variety of cellular and animal systems.
- Carmela Abraham, PhD, Normal aging and Alzheimer’s
- Lawreen Connors, PhD, Systemic amyloidosis
- Catherine Costello, PhD, Amyloidosis
- David A. Harris, MD, PhD, Prion diseases
- Peter Polgar, PhD, Vascular disease and aging
- Michael Sherman, PhD, Amyloidosis in Huntington’s
Signal Transduction & Cancer
Cancer is a class of diseases (also known as malignant neoplasms) in which normal cellular homeostasis is lost and a group of abnormal cells divide without control or stop responding to normal restraint in growth. In addition to uncontrolled growth, these cells can also display invasion (intrusion on and destruction of adjacent tissues) and sometimes metastasis. In the United States, cancer accounts for one of every four deaths. The American Cancer Society estimated that this year, about 565,650 Americans are expected to die of cancer, more than 1,500 people a day. Nearly all cancers are caused by abnormalities in the genetic material of the transformed cell. These abnormalities can either be inherited genetically (about 10% of cases) or occur sporadically due to the effects of carcinogens, such as tobacco smoke, radiation, chemicals, or infectious agents.
Genetic abnormalities found in cancer typically affect two general classes of genes: oncogenes and tumor suppressor genes. Cancer-promoting oncogenes are typically activated in cancer cells, giving those cells new properties, such as hyperactive growth and division, protection against programmed cell death, loss of respect for normal tissue boundaries, and the ability to become established in diverse tissue environments. Inactivation of tumor suppressor genes in cancer cells can result in the loss of normal functions in those cells, such as accurate DNA replication, control over the cell cycle, orientation and adhesion within tissues, and interaction with protective cells of the immune system. Additional pathways that contribute to tissue homeostasis are regulated by genes that control DNA damage, apoptosis, senescence, and the activity of carcinogens.
- Kathrin H. Kirsch, PhD, Cell signaling
- Zhijun Luo, PhD, Tumor growth and metabolism
- Valentina Perissi, PhD, Transcriptional coactivators
- Michael Sherman, PhD, Cell senescence, cell stress
- Bob Varelas, Development and cancer
Critical to the evolution of multicellular organisms was acquiring the ability to synthesize connections between cells. The extracellular matrix (ECM) integrates cells into tissues, tissues into organs, and organs into the organism. The ECM is an extension of the cell and participates actively in functions including development, migration, proliferation, metabolism and stabilization of tissue structure. Just as connective tissue was critical to the evolution of multicellular organisms, so too has evolution of multicellular organisms left them dependent upon connective tissue so that the ECM is associated with a wide range of diseases.
Cardiovascular disease is the number one cause of death in the United States. Vascular injury leads to chronic inflammation of the vasculature, causing atherosclerosis or lesion formation that leads to cardiovascular events. Likewise, injury and inflammation in the lung compromise its properties. Researchers in the Department of Biochemistry have identified basic elements of the mechanisms of vascular injury and lung fibrosis that contribute to cellular dysfunction, with emphasis on the role of the extracellular milieu.
- Matthew Layne, PhD, Transcriptional regulation, atherosclerosis, lung fibrosis
- Matthew Nugent, PhD, Glycosaminoglycans, atherosclerosis, chronic obstructive pulmonary disease
- Peter Polgar, PhD, Receptor structure/function
- Barbara Schreiber, PhD, Elastin, serum amyloid A, atherosclerosis
- Barbara Smith, PhD, Collagen, transcriptional regulation, atherosclerosis, lung fibrosis
- Phillip Stone, PhD, Elastin, pulmonary emphysema
- Vickery Trinkaus-Randall, PhD, glycosaminoglycans
- Joe Zaia, PhD, glycosaminoglycans
The modern world is in the midst of an obesity epidemic that is growing to the extent that, in 2003–2004, 32% of U.S. adults were obese and more than 50% were overweight, numbers that have been growing ever since. This dramatic increase in body weight has led to a significant upsurge in the number of individuals with obesity-related disorders, including Type-2 Diabetes, cardiovascular disease, hypertension, and dyslipidemia. A worrying trend is that adolescents are also becoming obese and, consequently, are succumbing to metabolic diseases that a decade ago occurred in adults only. Awareness of this trend has stirred a significant effort to understand more about the link between adiposity and metabolic disease.
Physiological control of metabolism involves an elaborately coordinated process involving cross-talk between several organs and tissues that regulate the production of hormones and the metabolism of lipids and glucose. In an effort to gain a greater understanding of the control of energy balance, investigators in the Department of Biochemistry are attempting to identify the molecular mechanisms within each tissue that contribute to the overall control of metabolism. This research has included defining the signaling pathways and transcriptional events that specify production and action of metabolically important hormones and cytokines.
- Stephen R. Farmer, PhD, Transcriptional control of adipocyte formation and function
- Konstantin Kandror, PhD, Cell biological aspects of insulin signaling
- Matthew Layne, PhD, Adipose tissue formation and fibrosis
- Valentina Perissi, PhD, Transcriptional coactivators
- Paul F. Pilch, PhD, Vesicular traffic related to insulin action, caveolae, lipodystrophies
- Barbara Schreiber, PhD, Inflammation and smooth muscle cell lipid metabolism
Proteomics & Glycomics
Proteins, carbohydrates, and lipids serve both structural and signaling roles; their identities and distributions vary with growth, development, and disease. At cell and membrane surfaces and in the extracellular space, the interactions of cells are regulated by these classes of molecules. Within cells, they govern traffic between compartments.
Proteomics, glycomics, and lipidomics investigate the phenotypes with respect to these compound classes in a given cell, tissue, or organism, and the dynamics of their expression related to biological transformation, thus leading to understanding of intracellular and intercellular processes at the level of expression rather than extrapolation from genetic information. These studies are relevant to metabolic disorders and diseases such as diabetes, oxidative stress, cancers, neurological disorders, infectious diseases, and atherosclerosis, as well as normal development and aging.
- Catherine Costello, PhD, Proteins, glycans and lipids
- Cheng Lin, PhD, Proteins, glycans
- Joseph Zaia, PhD, Glycosaminoglycans, protein-GAG interactions
Directed cell migration plays a critical role in embryonic development. To migrate in a directed way, a cell must be able to detect and move towards a source of an attractive signal (chemoattractant) or away from a repulsive one. This requires the creation of spatially asymmetrical signaling that leads to extension of leading edge protrusions such as lamellipodia, the generation of traction and force, and a balance of detachment and attachment to neighboring cells and the extracellular matrix. Thus, there is a constant need for the cell to coordinate a variety of extracellular and intracellular activities both spatially and temporally. The challenge is to understand how the cell compartmentalizes, yet cooperatively couples, these activities to drive directed cell movement and how upstream signaling controls this behavior. Toward this end, investigators in the Department of Biochemistry study growth factor signaling that is modulated by specific extracellular matrix proteins and induces specific changes in cellular architecture. In vivo and three-dimensional ex vivo models are studied in which growth factor signaling and downstream effectors are modulated through introduction of mutant forms, and resultant morphology and cell migration are analyzed.
- Matthew Nugent, PhD, Proteoglycans, growth factors, ECM
- Barbara M. Schreiber, PhD, Vascular development, ECM
- Karen Symes, PhD, Cell migration, notochord development, PDGF signaling
- Vickery Trinkaus-Randall, PhD, EGF receptor, glycosaminoglycans
- Bob Varelas, PhD, Development and cancer
Students are an important and integral part of any educational department and this is no different at BUSM’s Department of Biochemistry. In order to be more involved in departmental affairs, students of the department have created the Biochemistry Student Organization (BSO) to foster the academic and professional development of the student body. In addition to this primary mission, the BSO also organizes and sponsors various social and academic events for students and the department. Our students are also active in the Division of Graduate Medical Sciences Student Organization (GMSSO), an organization that encompasses students in all programs throughout the Division of Graduate Medical Sciences.