Area:
Dopamine and Serotonin Agonists
We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Deborah M. Kurrasch-Orbaugh is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 2003 — 2005 |
Kurrasch-Orbaugh, Deborah M |
F32Activity Code Description:
To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Characterizing Rgs Mutations in Cardiomyopathy @ University of Texas SW Med Ctr/Dallas
[unreadable] DESCRIPTION (provided by applicant): The hypothesis of this proposal is that the RGS 16 protein is an integral component of the G-alpha-q/11 signaling complex, serving as a feedback inhibitor of G-alpha-q/11 signaling in stressed cardiomyocytes, thus helping to maintain cardiac homeostasis. We propose that a point mutation in the RGS box of RGS16 (D179Y) found in patients with dilated cardiomyopathy alters the conformation of the interaction surface with G-alpha-q/11 and/or other proteins in the signaling complex, rendering RGS16 D179Y to function as a dominant negative protein, ultimately contributing to dilated cardiomyopathy. To test this hypothesis, we shall explore the following specific aims: Aim 1. We shall examine the GAP and potential dominant negative activity of D179Y and wild type RGS16 proteins in several in vitro assays, including single-turnover assays, transition-state analog binding assays, and G-alpha-q -Coupled steady state assays, and G-alpha-q -coupled MAPK activation; Aim 2. We will overexpress D179Y and RGS 16 proteins specifically in cardiomyocytes by employing the alpha-MHC promoter in transgenic mice and then characterize the onset of cardiomyocytes hypertrophy; Aim 3. We will create Rgs 16 D179Y knock-in mice and characterize the onset of dilated cardiomyopathy; Aim 4. We will continue to screen cardiac patients and healthy individuals to identify additional Rgs mutation. The primary objective of this proposal is to evaluate the causative role of the D179Y allele of RGS16 in the progression of dilated cardiomyopathy. [unreadable] [unreadable] [unreadable] [unreadable]
|
0.961 |