Area:
Molecular Biology, Cell Biology, Genetics
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High-probability grants
According to our matching algorithm, Jay E. Brenman is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2006 — 2010 |
Brenman, Jay |
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. |
Genetic Analysis of Dendrite and Dendritic Filopodia Formation @ University of North Carolina Chapel Hill
[unreadable] DESCRIPTION (provided by applicant): [unreadable] In the brain, most information processing physically occurs on neuronal dendrites. Understanding how dendrites and dendritic structure develop and function is critical to understanding normal cognition and what may be perturbed in human cognitive disorders and retardation syndromes. Evidence for altered dendritic morphology exists in Alzheimers, Fragile X, and Downs syndrome. In some vertebrates there is evidence that dendritic filopodia help form dendritic arbors. In mammals, at least some dendritic filopodia can become dendritic spines. In Drosophila, we are able to visualize dendrites and dendritic filopodia in optically transparent intact animals. We believe the study of dendrites and dendritic filopodia development using a simple but powerful genetic model, should yield insights into more complex mammalian dendrite development. Our approach combines a genetically amenable organism, Drosophila, with high-resolution microscopy to perform large-scale forward genetics to identify genes and signaling pathways regulating dendritic development. We are also investigating the roles of CaMKII, a molecule implicated in learning and memory, as a potent regulator of dendritic structure in Drosophila. As 72% of all human neurological disease genes are found in Drosophila, orthologues of such genes identified herein may be candidates to play a role in mammalian dendrite development and potentially human disease. [unreadable] [unreadable] [unreadable]
|
0.915 |
2009 |
Brenman, Jay Sexton, Jonathan Zachary (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.) |
Hts Assay Development to Identify Regulators of Peroxisome Biogenesis/Function @ Univ of North Carolina Chapel Hill
DESCRIPTION (provided by applicant): This proposal seeks to use chemical genomics to identify small-molecule compounds that modulate peroxisome biogenesis and function. Peroxisomes are major sites of fatty-acid oxidation and the only site of very long-chain fatty-acid metabolism. Ectopic fatty-acid deposition in non-adipose tissue leads to lipotoxicity, which is associated with numerous disease conditions. Increasing fatty-acid oxidation capacity in cells and shifting fatty- acid metabolism towards oxidation may prevent lipotoxicity and could be therapeutic. In addition, peroxisomes are required for the synthesis of specialized phospholipids, sphingolipids, that are required in myelin and when absent result in neurodegenerative diseases. In fact, multiple human diseases ranging from neurodegeneration to metabolic abnormalities result from the absence of functional peroxisomes. We are developing a novel high throughput screening (HTS) assay using human liver cells expressing a fluorescent peroxisome reporter to monitor peroxisome biogenesis in real time. Compounds identified our screen could be the first step towards developing PPAR independent potential therapeutics for diseases ranging from Type 2 diabetes to neurodegenerative conditions. PUBLIC HEALTH RELEVANCE: This proposal utilizes a novel high throughput screening (HTS) assay to identify novel PPAR independent regulators of peroxisome biogenesis and function. Due to peroxisomes required function for sphingolipid synthesis, which are required for myelination, decreased peroxisome function results in neurodegenerative disease (e.g. Zellwegers syndrome). The compounds identified from this proposal are a first step towards developing potential therapeutics for neurodegenerative disease, metabolic syndrome, and Type 2 diabetes.
|
0.903 |
2012 — 2016 |
Brenman, Jay |
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. |
Genetic Elucidation of Amp-Activated Protein Kinase Signaling Mechanisms @ Univ of North Carolina Chapel Hill
Abstract: AMP-activated protein kinase (AMPK) functions as a key energy sensor and metabolic rheostat to maintain cells' energy needs, largely through maintaining ATP levels. Disruption of AMPK signaling leads to neuronal death, while mutations in human AMPK subunits cause the fatal cardiac disorder, Wolff-Parkinson-White syndrome. We are using a genetic model in Drosophila to identify genes that modulate AMPK signaling in vivo. Using this novel forward genetic screen we have identified nucleoside diphosphate kinase (NDPK) as a potential modifier and target of AMPK signaling. We have found a new mechanism whereby AMPK-dependent phsphorylation of NDPK turns it off. This off switch site corresponds to a location mutated in advanced human neuroblastoma. Through identification of new genes that suppress AMPK RNAi lethality, and making a genetic model of mutations in AMPK that cause human disease, we hope to identify both new mechanisms and molecules that modulate AMPK function in vivo.
|
0.903 |