Area:
Cell Biology, Molecular Biology, Human Development
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High-probability grants
According to our matching algorithm, Ricardo A. Feldman is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1991 — 1997 |
Feldman, Ricardo A |
R29Activity Code Description: Undocumented code - click on the grant title for more information. |
Fps/Fes Proto-Oncogene in Myeloid Cell Function @ University of Maryland Baltimore
The c-fps/fes gene encodes a cytoplasmic tyrosine kinase that is specifically expressed in myeloid cells, in particular in macrophages. The long-term objective of this study is to understand the biological role and mechanism of action of this gene, and the molecular basis of its oncogenic potential. We will investigate the possible role of c-fps/fes in signal transduction by determining if its product undergoes any biochemical changes (i.e. tyrosine phosphorylation and activation of enzymatic activity) during myeloid cell differentiation and macrophage activation, and by examining the biological and biochemical effects of reintroducing biologically active fps/fes genes into these cells. The biochemical parameters of c-fps/fes action will be dissected using temperature sensitive and other mutants of c-fps/fes, which will be introduced into myeloid cells capable of undergoing differentiation and maturation by retroviral mediated gene transfer. These experiments should clarify the biological functions of c-fps/fes and provide the means to identify proliferation-, differentiation-, and maturation-specific substrates. We will also generate antibodies against two previously identified substrates of c-fps/fes, which will be used for their characterization and molecular cloning. We will identify cellular proteins that interact with c-fps/fes kinase using purified c-fps/fes protein expressed in baculovirus, and functional domains expressed in bacteria, as affinity reagents. These proteins will also be used to generate specific monoclonal and polyclonal antibodies, which will be used in conjunction with fps/fes mutants to study functional interactions of c-fps/fes kinase with substrates and other cellular proteins. The c-fps/fes product has unique biological and biochemical properties. The elucidation of its mechanism of action will shed light on the role of tyrosine phosphorylation in myeloid cell differentiation and macrophage activation. As macrophage activation plays a central role in the immune response to infections, and as new experimental therapies rely on the use of myeloid CSFs that utilize tyrosine phosphorylation pathways to achieve differentiation of leukemic cells, the mechanisms uncovered in these studies have broad potential clinical implications.
|
0.972 |
1998 — 2004 |
Feldman, Ricardo A |
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. |
Role of Fps/Fes Proto-Oncogene in Myeloid Cell Function @ University of Maryland Baltimore
The long-term objective of this study is to understand the biological role and mechanism of action of the c-fps/Fes proto-oncogene. Fes encodes a cytoplasmic tyrosine kinase that is specifically expressed in myeloid cells. We have obtained evidence that Fes is involved in signaling through a specialized class of surface receptors during cell- cell and cell-matrix interactions, and suggests a possible role of Fes in mediating the release of inflammatory cytokines during macrophage activation. We found that VLA-4 integrin engagement in macrophages, a process that induces the release of inflammatory mediators, results in the activation of Fes kinase. We have also identified a number of macrophage specific substrates of Fes, which are involved in cell adhesion and regulation of inflammatory cytokines. One of the substrates phosphorylated by Fes is the crk-associated substrates (Cas) and another is a new 130 kDa protein (P130). Cas is an adapter protein involved in integrin signalling. P130 is a protein expressed only in hematopoietic cells and has been implicated in release of inflammatory cytokines. We hypothesize that Fes is involved in a novel integrin- dependent pathway that regulates the release of inflammatory mediators. In this proposal we will study the mechanism by which integrin engagement results in activation of Fes kinase, and how phosphorylation of its specific substrates regulates the inflammatory response of macrophages. The macrophage adhesion receptor VLA-4 will be engaged by cross-linking with specific antibodies and by adhesions to fibronectin, and the functional interactions between Fes and the integrin cascade will be examined. Using a combination of genetic and biochemical approaches we will elucidate the mechanisms involved in Fes kinase activation, characterize the Fes substrates, identify its downstream targets, and analyze the role of Fes in the adhesion-dependent macrophage inflammatory response. Finally, we will identify the transcriptional regulators activated by Fes and map the Fes-responsive elements in the promoters of genes under Fes control. Macrophages are a central player in the immune response to microorganisms, in tumoricidal activity, and in pathological conditions such as atherosclerosis. The proposed investigation will bring to light a previously unknown regulatory cascade involved in inflammatory response of macrophage. This will have an impact on the rational design of therapies aimed at preventing the inappropriate activation of macrophages, a biomedical problem of paramount importance.
|
0.972 |
2012 — 2013 |
Feldman, Ricardo A Hong, L Elliot [⬀] O'donnell, Patricio (co-PI) [⬀] |
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.) |
Cellular Electrophysiology of Nicotine Addiction Clinical Phenotypes @ University of Maryland Baltimore
DESCRIPTION (provided by applicant): Smoking remains the leading cause of preventable diseases and death in the US, and is known to be heritable. This application aims to develop a set of nicotine addiction cell lines based on clinically defined imaging phenotype and genotype. Our goal is to test that neuronal electrophysiological response to nicotinic agonists will be associated with the strength of the clinical imaging based circuit phenotype in patients with severe nicotine addiction and carry smoking related risk alleles. Our innovation here is to closely link these cell lines with state-of-the art clinical measures of nicotine addiction, so that we coud iteratively test electrophysiological phenotypes of the cells that are likely underlying key clinicl nicotine addiction measures.
|
0.972 |