The study of the inner nuclear membrane proteins is emerging as an exciting new field in biology because of the impact these proteins may have in development. We have recently shown that the inner nuclear membrane protein MAN1 can repress TGF-beta, BMP and activin signaling through its interaction with the Smad proteins. This is supported by studies showing that mutations in MAN1 that produce truncated proteins incapable of binding to Smad block TGF-beta superfamily signaling resulting in osteopoikilosis, Buschke-Ollendorff syndrome and melorheostosis. Taking a biochemical and cell biological approach, this research will explore the function of MAN1 in the regulation of TGF-beta superfamily signaling, trying to elucidate the exact mechanism by which this inner nuclear membrane protein regulates TGF-beta superfamily signaling from the inner nuclear membrane.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31GM077101-03
Application #
7325769
Study Section
Special Emphasis Panel (ZRG1-GGG-G (29))
Program Officer
Toliver, Adolphus
Project Start
2006-01-01
Project End
2008-04-30
Budget Start
2008-01-01
Budget End
2008-04-30
Support Year
3
Fiscal Year
2008
Total Cost
$10,556
Indirect Cost
Name
University of California Berkeley
Department
Biochemistry
Type
Schools of Arts and Sciences
DUNS #
124726725
City
Berkeley
State
CA
Country
United States
Zip Code
94704