CONGRATULATIONS to Adrian Salic, Assistant Professor in the Dept of Cell Biology, who is the recipient of the 2010 R.R. Bensley Award in Cell Biology from the American Society of Anatomists.
Adrian Salic
This award recognizes a cell biologist whose publications have had substantial impact on his/her field and has made a distinguished contribution to the advancement of anatomy through discovery, ingenuity, and publications in the field of cell biology. The Salic laboratory studies biochemical and cellular mechanisms involved in signal transduction through the Hedgehog signaling pathway and also develops and applies new chemical technologies to study the cell biology of lipids.
CONGRATULATIONS to Alfred Goldberg, Professor in the Department of Cell Biology, who has been elected to the Institute of Medicine of the National Academy of Sciences.
A.Goldberg
Alfred Goldberg has been associated with Harvard during his entire academic career: he earned his A. B. in 1963 and his Ph.D. in 1968 from Harvard University and was appointed an Assistant Professor at Harvard Medical School in 1969, immediately following one year as an Instructor. Dr. Goldberg has been a Professor at Harvard Medical School since 1977. The Goldberg laboratory is presently studying the regulation and mechanisms of protein breakdown in animal and bacterial cells
Flanagan lab in Dept of Cell Biology identifies ligand-receptor interaction that may provide a therapeutic target for drugs that would potentially promote nerve growth and regeneration after brain and spinal cord injury, and may be applicable to other diseases such as neurodegeneration and stroke.
J. Flanagan
After spinal cord injuries, recovery is minimal. At the site of injury, a scar forms which acts as a double-edged sword—it can save a victim’s life by preventing the injury from spreading, yet seal his or her fate as a paraplegic or quadriplegic by blocking nerve regeneration. Cells in the scar produce a family of molecules known as chondroitin sulfate proteoglycans (CSPGs) which can inhibit nerve fibers from growing past the injury site to connect with their original targets. Although this inhibitory action of the CSPGs has been known for two decades, no corresponding receptor has been found on the neurons, and it has been unclear if they even act via a specific receptor, limiting molecular progress in this area. In a recent paper from the Flanagan lab a transmembrane protein tyrosine phosphatase, PTPσ, was identified as a receptor for neural CSPGs (Shen et al., Science 2009). Binding involves the chondroitin sulfate chains and a specific site on the first immunoglobulin-like domain of PTPσ. In culture, PTPσ–/– neurons showed reduced inhibition by CSPG. A PTPσ fusion protein probe can detect cognate ligands that are up-regulated specifically at neural lesion sites. After spinal cord injury, PTPσ gene disruption enhanced the ability of axons to penetrate regions containing CSPG.