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High-probability grants
According to our matching algorithm, David M. Feliciano is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2011 — 2013 |
Feliciano, David Matthew |
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. |
Role of Perinatal Neuronal Stem Cells in Tuber Formation
DESCRIPTION (provided by applicant): Tuberous Sclerosis Complex (TSC) is a severe genetic disorder characterized by angiofibroma, mental retardation, and epilepsy, the latter of which likely results from benign malformations known as hamartias and hamartomas. Inactivating mutations in one of two tumor suppressor genes, TSC1 and TSC2, which encode hamartin and tuberin respectively, are thought to underlie the neurological lesions associated with TSC. Although the molecular functions of TSC1 and TSC2 as a negative regulator of the mTOR kinase pathway are well established, there remains considerable confusion as to how TSC gene inactivation results in neurological lesions. The uncertainty of how TSC mutation can result in such gross neurological pathologies stems in part, from the inability to form a viable animal model which faithfully represents the human pathology. Brain lesions in TSC appear to result from a defect in neural progenitor development. For example, hamartias known as cortical tubers are thought to arise during the mid-gestational periods of corticogenesis from radial glia. Tubers can indeed be detected as early as 19 weeks of gestation in humans. In the majority of the cases, tubers affect only a restricted region of the cerebral cortex, suggesting that they form in later rather than earlier periods of cortical development. This proposal seeks to identify a role for TSC1 in radial glia of the perinatal ventricular zone. Biallelic inactivation of a viable TSC1 copy in the presence of an inherited mutant TSC1 during embryonic development will be induced by in utero electroporations. Resulting lesions will be examined to determine the extent to which they recapitulate the human TSC pathology and to identify whether hyper-excitability originates in surrounding tissue, or within the lesion itself. PUBLIC HEALTH RELEVANCE: Tuberous sclerosis complex (TSC) is a multisystem genetic disorder with a preponderance of seizures which are associated with focal cortical lesions known as tubers. TSC is unique in that tubers are readily identified and are often targeted for surgical resection. I propose to develop a novel model of TSC with discreet neurological lesions having features of cortical tubers for which I will measure electrophysiological properties.
|
0.97 |
2016 |
Feliciano, David Matthew |
R15Activity Code Description: Supports small-scale research projects at educational institutions that provide baccalaureate or advanced degrees for a significant number of the Nation’s research scientists but that have not been major recipients of NIH support. The goals of the program are to (1) support meritorious research, (2) expose students to research, and (3) strengthen the research environment of the institution. Awards provide limited Direct Costs, plus applicable F&A costs, for periods not to exceed 36 months. This activity code uses multi-year funding authority; however, OER approval is NOT needed prior to an IC using this activity code. |
Slc7a5-Mtor Regulation of Neural Development
Project Summary The causes of autism spectrum disorders and of epilepsy are poorly understood. A major genetic link to these neurodevelopmental disorders is the mTOR pathway. mTOR is a protein kinase that regulates translation and autophagy. This proposal seeks to test the hypothesis that a transporter of amino acids regulates the mTOR pathway in newborn neurons during cerebral cortical development. Patients that harbor copy number variations or with mutations that ultimately effect the expression of this gene present with a spectrum of neuropathological manifestations including epilepsy, autism, and intellectual delay. While the precise association of the amino acid transporter with the manifestations is still unknown, here we propose that changes in expression alter mTOR activity and neuron morphology. In aim 1 we propose to determine whether and at what times in development the transporter regulates mTOR pathway. Additional experiments include examining the downstream pathways and cellular consequences of manipulating the transporter. In aim 2 we propose to examine the cellular consequences of altering expression of the amino acid transporter. More specifically, we plan to examine neuron morphology including dendrite arborization in vivo following over- expression or knockdown of the transporter. In aim 3 we propose to determine whether morphological changes caused by manipulations of the transporter are due to aberrant mTOR pathway activity. We first will perform experiments using reversible shRNAs and shRNA resistant constructs to define the extent and timing for which morphology can be rescued. Finally, we will define whether changes in neuron morphology caused by aberrant expression of the transporter can be reversed or prevented by manipulating the mTOR pathway.
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1 |