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TSC Signaling: Implications for the treatment of Lymphangioleiomyomatosis (LAM) and Tuberous Sclerosis Complex (TSC)
Dr. David Sabatini is Associate Professor of Biology at MIT. Dr. Sabatini has done seminal work
on mechanisms that control cell growth, including on the mTOR pathway. His lab has linked
to a cell's ability to sense nutrients in its environment.
Dr. Brendan Manning is Associate Professor of Genetics and Complex Disease at the Harvard School of Public Health.
Research in his laboratory is focused on cell signaling pathways underlying tumorigenesis and metabolic diseases.
A major aim of this research is to define signaling defects caused by the loss of the TSC1 and TSC2 tumor
suppressors, which are mutated in tuberous sclerosis complex and lymphangioleiomyomatosis.
Date: Thursday, October 26, 2006 5:00-7:00 PM
Location: New Research Building, Harvard Medical School
77 Avenue Louis Pasteur, Room 350
Parking: Free parking in the lot below the New Research Building has been graciously donated. Space is limited
and will be made available to participants coming from outside of the Longwood Medical Area, if requested
by Tuesday, October 24, 2006.
Please RSVP to amy_farber@hms.harvard.edu and indicate the number of people attending.
We appreciate your help in forwarding this announcement to relevant researchers, labs, and clinicians.
Thank you for your interest and participation. We look forward to seeing you on Thursday, October 26, 2006.
Best regards,
David Kwiatkowski, Amy Farber and Michael Nurok
Click here for the overview of the meeting
Background Research on this month's topic:
Click here to view Dr. Manning's Powerpoint File Online
Click here to view Dr. Sabatini's Power Point File Online
Click here to download Dr. Manning's Powerpoint file to your desktop
Click here to download Dr. Sabatini's Powerpoint file to your desktop
Dr. Brendan Manning's suggested readings:
- Feedback inhibition of Akt signaling limits the growth of tumors lacking Tsc2
- Identification of the Tuberous Sclerosis Complex-2 Tumor Suppressor Gene Product Tuberin as a Target of the Phosphoinositide 3-Kinase/Akt Pathway
- Rheb fills a GAP between TSC and TOR
- S6K1 Regulates GSK3 under Conditions of mTOR-Dependent Feedback Inhibition of Akt
- Balancing Akt with S6K: implications for both metabolic diseases and tumorigenesis
- Pubmed citations
Dr David Sabatini's suggested readings:
