We will investigate the role of activin signaling in controlling pituitary gonadotrope gene expression and physiology in vivo in transgenic mice.
Specific Aim 1 Investigate kinase-deficient type II, IIB, and IB receptors for their activity in blocking activin action in alphaT3-1 cells to further understand the role of activin in the gonadotrope and to choose the optimal dominant negative receptor for creating transgenic mice.
Specific Aim 2 Create and characterize transgenic mice in which the activin signaling mechanisms have been disrupted in the gonadotrope.
Specific Aim 3 Determine the role of activin signaling in the gonadotrope in vivo utilizing transgenic mice in which pituitary activin signaling mechanisms have been specifically disrupted. The results of these studies will lead to a more thorough understanding of the molecular mechanisms involved in regulating reproductive function.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32HD008560-01A1
Application #
6062486
Study Section
Endocrinology Study Section (END)
Program Officer
De Paolo, Louis V
Project Start
2000-08-08
Project End
Budget Start
2000-02-07
Budget End
2001-02-06
Support Year
1
Fiscal Year
2000
Total Cost
$32,416
Indirect Cost
Name
University of California San Diego
Department
Obstetrics & Gynecology
Type
Schools of Medicine
DUNS #
077758407
City
La Jolla
State
CA
Country
United States
Zip Code
92093