Department of
Biological Chemistry & Molecular Pharmacology

Cell physiology

David Golan

Professor
Telephone: 
617- 432- 2256
Fax: 
617-432- 3833
Address: 
Room SGM - 304C
Address: 
240 Longwood Avenue
Address: 
Boston MA 02115

Our goals are to understand the molecular interactions controlling protein and lipid mobility and distribution in cell membranes, the roles these mechanisms play in interactions between cells, and the relationships between derangements in these mechanisms and the pathophysiology of disease. We have designed and constructed several time-resolved scanning laser microscopes for interactive monitoring, tracking, and manipulating of biological samples at the single-cell and single-molecule levels on the µs-ms time scale and nm distance scale. Using these instruments, we are investigating: 1) Molecular interactions in erythroid cell membranes.

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Ed Harlow

Professor

Research in the Harlow laboratory focuses on new approaches for functional analysis in mammalian cells. Our primary interest is learning how to do high throughput and unbiased screens for genes that affect key phenotypes of cancer biology. The levels of specific proteins can be increased or decreased by expressing the protein itself from a cDNA copy or by the introduction of an inhibitory RNA for the mRNA. We use libraries of individually cloned and sequenced full length coding regions and siRNAs to raise or lower protein levels in cells and study changes in cellular phenotypes. At present we have a complete proteome for several test organisms—bacteria Pseudomonas aeruginosa, the yeast Saccharomyces cerevisiae, and libraries for several viruses.

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Steven E. Shoelson

Professor
Telephone: 
617-732-2528
Fax: 
617-735-1970
Address: 
Dept. of Medicine
Address: 
Joslin Diabetes Center
Address: 
One Joslin Place
Address: 
Boston, MA 02115

Our studies can be divided into two main areas, (1) pathophysiological mechanisms of insulin resistance and type 2 diabetes, and (2) structural biology of diabetes and obesity. Type 1 or insulin-dependent diabetes is caused by insulin deficiency, in most cases due to autoimmune destruction of pancreatic beta cells. Fewer than 1 in 10 diabetics have this more severe form of the disease. Type 2 diabetes is much more common, and its prevalence is rapidly rising. Type 2 diabetes or NIDDM, affects greater than 10% of our population. In type 2 diabetes insulin is present, often in excess, but target tissues fail to respond appropriately. This is referred to as insulin resistance, a problem in signal transduction.

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