Area:
Molecular Biology, Cell Biology
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, Thomas J. McGarry is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1996 — 1998 |
Mcgarry, Thomas J |
K08Activity Code Description: To provide the opportunity for promising medical scientists with demonstrated aptitude to develop into independent investigators, or for faculty members to pursue research aspects of categorical areas applicable to the awarding unit, and aid in filling the academic faculty gap in these shortage areas within health profession's institutions of the country. |
Protein Degradation During Mitosis and Development @ Harvard University (Medical School) |
0.942 |
2008 — 2009 |
Mcgarry, Thomas J |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
The Role of Geminin in Hematopoiesis @ Northwestern University
[unreadable] DESCRIPTION (provided by applicant): Hematopoietic stem cells (HSCs) in the bone marrow supply the circulation with mature blood cells throughout life. Division of the HSCs both replenishes their own numbers and provides committed progenitor cells that give rise to the erythrocyte, leukocyte, and megakaryocyte lineages. Progenitor cells undergo a limited number of divisions then differentiate into mature blood cells. Progenitor cell division and differentiation must be carefully balanced in order to provide the correct numbers and proportions of mature cells. Imbalances between proliferation and differentiation underlie common hematological problems like leukemia, lymphoma, and myelodysplastic syndromes. Despite their obvious importance, the mechanisms that control the choice between continued cell division and terminal differentiation are largely unknown. This project will examine the role of the regulatory protein Geminin in the proliferation and differentiation of hematopoietic cells. Geminin is required for pluripotency and is thought to maintain dividing cells in an undifferentiated state. Geminin is a bi-functional protein that controls the extent of DNA replication and inhibits homeodomain (Hox) transcription factors that are known to be crucial regulators of hematopoiesis. Geminin knockdown activates the Fanconi Anemia pathway, and over- expression of the replication factor inhibited by Geminin, Cdt1, in p53-/- T cells accelerates the development of lymphoblastic lymphoma. We are using a conditional knockout strategy to investigate the role of Geminin in definitive hematopoiesis. Gene-targeted mice, in which LoxP sites flank the essential exons of the Geminin gene, are being bred to mice that express Cre recombinase under the control of the interferon-inducible Mx-1 promoter. These mice will be treated with polyinosine- polycytidine (poly I:C) to induce Cre recombinase and delete the Geminin gene in hematopoietic cells. We will determine how Geminin loss affects the pattern of cell division and differentiation in the bone marrow, how Geminin regulates the cell cycle of hematopoietic cells, and whether Geminin suppresses the development of leukemias or lymphomas. We hope to gain a more complete understanding of normal hematopoiesis and identify a new target for therapy of hematological malignancies. PROJECT NARRATIVE Stem cells in the bone marrow continually divide throughout a person's life in order to produce mature blood cells. Problems in the division or the maturation of the growing blood cells give rise to leukemia and lymphoma, two of the most common cancers. This project examines the role of the protein Geminin in controlling blood cell development. [unreadable] [unreadable] [unreadable] [unreadable]
|
1 |
2009 — 2010 |
Mcgarry, Thomas J |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Creation of Stem Cells by Nuclear Reprogramming @ Northwestern University At Chicago
DESCRIPTION (provided by applicant): Each year approximately 900,000 Americans suffer a myocardial infarction. Approximately 225,000 of these victims die and the others are at risk for chronic complications, including congestive heart failure and intractable ventricular arrhythmias. Unlike other organs such as the liver, the heart is unable to regenerate and replace the lost myocardial cells to any significant extent. Much effort is now being expended to find ways to induce, stimulate, and augment myocardial regeneration. One promising approach is transplantation of undifferentiated stem cells into the infracted zone. One bottleneck in stem cell transplantation is the acquisition of a sufficient number of stem cells to be infused into the patient. There is much interest in using donor cells that are derivatives of embryonic stem cells (ES cells). Because of ethical concerns about destroying human embryos, much attention has been focused on obtaining ES cells by other means. One potential solution is to reprogram a patient's own somatic cells so that they become more like stem cells. Nuclear reprogramming the process by which the nucleus of terminally differentiated cells becomes more like the nucleus of an undifferentiated stem cell. The goal of the experiments in this proposal is to reprogram differentiated cells with extracts of Xenopus eggs. Our approach will be to expose permeabilized cells to concentrated egg extracts then assay the extent of reprogramming by transplanting them into enucleated Xenopus eggs. Reprogramming will be indicated by improved development of eggs that receive extract-treated nuclei compared to those that receive untreated nuclei. If we can demonstrate reprogramming by extracts, then we can investigate various reprogramming models by treating the extract with inhibitors or eliminating specific proteins by immunodepletion. It may even be possible to purify protein complexes with reprogramming activity. The results of our studies will shed light on the nature of the epigenetic changes that drive cell differentiation. We also hope to develop extracts that efficiently reprogram differentiated cells so that they can be used for cell replacement therapy. PUBLIC HEALTH RELEVANCE: Heart attack survivors are at risk for developing heart failure because the heart cannot repair and regenerate itself like some other organs. In recent years, heart attack victims have been treated with stem cells in the hope that these will be able to turn into heart muscle cells and restore the heart's pumping function. The purpose of this proposal is to treat normal cells with extracts of egg cells to see if they can be turned into stem cells in the hope that these can be used to repair the heart.
|
1 |