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, Teresa M Wilson is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1997 — 1998 |
Wilson, Teresa 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. |
Human Mismatch Repair Protein Hmsh2 @ Thomas Jefferson University
DNA binding protein; protein structure function; DNA repair; neoplasm /cancer genetics; colorectal neoplasms; transfection /expression vector; enzyme activity; adenosinetriphosphatase; DNA damage; human genetic material tag; tissue /cell culture; molecular cloning;
|
0.931 |
2003 — 2007 |
Wilson, Teresa M |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Acetylation of the Human Exonuclease 1 Protein @ University of Maryland Baltimore
Principal Investigator/Program Director (Last, first, middle): Wilson, Teresa, M PROJECT SUMMARY/ABSTRACT The most important risk factor for the development of colorectal cancer is age: greater than 90% of people diagnosed with colorectal cancer are 50 or older. A gender-based difference exists as well. With considerations for age and race/ethnicity, colorectal cancer incidence and mortality rates are more than 35% higher in men than in women. Age and gender also affect the occurrence of microsatellite instability (MSI), a hallmark of defects in the mismatch repair pathway (MMR), in both sporadic and inherited colorectal tumors. Women in general are less likely than men to have MSI positive tumors at a young age, a trend that is maintained in older women undergoing hormone replacement therapy. The MMR pathway performs a critical role in the maintenance of genomic stability by repairing mismatches and insertion/deletion loops in DNA and by signaling for programmed cell death in response to DNA damage. We have found that MMR deficient cells are more resistant to apoptosis and cell death induced by treatment with estrogen. Additionally, we have found that estrogen enhances the interaction between the estrogen receptor beta (ER), the major ER isoform in the colon, and the MMR lesion recognition complexes. The main goal of this proposal is to test the hypothesis that ER, estrogen, and the human mismatch repair proteins function together to maintain genomic integrity. This will be accomplished in three Specific Aims: (1) Specific Aim 1 will test the hypothesis that estrogen and ER enhance the mismatch repair-dependent cellular response to DNA damage; (2) Specific Aim 2 will test the hypothesis that E2 and ER enhance MMR DNA repair activities; and (3) Specific Aim 3 will test the hypothesis that the MMR proteins modulate the biochemical activities of ER. Project Description Page 6
|
0.934 |