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High-probability grants
According to our matching algorithm, Dianna E. Willis is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2005 — 2007 |
Willis, Dianna E. |
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. |
Mrna Transport and Local Translation After Axotomy @ Alfred I. Du Pont Hosp For Children
DESCRIPTION (provided by applicant): Neurons can spatially regulate gene expression by targeting mRNAs to subcellular domains to locally generate new proteins. Although best characterized in the dendritic compartment, recent studies have proven that the axonal compartment is also capable of local protein synthesis. This localized axonal protein synthesis is regulated by extracellular stimuli that alter axonal growth. From proteomics-based studies, we have identified a substantial number of proteins that are synthesized in the regenerating axons of cultured DRG neurons. This new knowledge of the proteins that are locally synthesized in axons allows us to ask how transport of mRNAs and translation of specific mRNAs is regulated in the axons. The central hypothesis of this proposal is that neurons modulate the protein makeup of axonal subdomains in response to environmental cues by specifically altering transport of mRNAs into, and synthesis of new proteins directly in, growing axons. I will test this hypothesis with two specific aims. First, I will address the regulation of axonal mRNA trafficking by extracellular stimuli and test the hypothesis that transport of mRNAs into the regenerating axon is modulated by extracellular signals acting through receptor-mediated signal transduction pathways. Second, I will test the specificity of intra-axonal protein synthesis and the hypothesis that axonal protein synthesis is differentially regulated by environmental stimuli. I will focus these analyses on axonal mRNAs encoding structural proteins (Beta-actin, peripherin and vimentin) and injury-response proteins (HSP70, grp78/BiP and Importin Beta1) that play central roles in axonal growth.
|
0.904 |
2007 — 2012 |
Willis, Dianna E. |
K99Activity Code Description: To support the initial phase of a Career/Research Transition award program that provides 1-2 years of mentored support for highly motivated, advanced postdoctoral research scientists. R00Activity Code Description: To support the second phase of a Career/Research Transition award program that provides 1 -3 years of independent research support (R00) contingent on securing an independent research position. Award recipients will be expected to compete successfully for independent R01 support from the NIH during the R00 research transition award period. |
Axonal Transport and Local Translation in Neuropathic Pain @ Alfred I. Du Pont Hosp For Children
[unreadable] DESCRIPTION (provided by applicant): [unreadable] [unreadable] Localized protein synthesis provides a means for the distal processes of the neuron to rapidly and autonomously respond to its environment. Although best characterized in the dendritic compartment, work over the past 5 years has proven that axons are capable of locally generating new proteins. In dendrites, activity-dependent local protein synthesis plays a role in synaptic plasticity. There is also evidence for activity-dependent protein synthesis in axons. Given the complex population of proteins synthesized in axons, it is likely that axonally synthesized proteins also play a role in the function of mature axons. The central hypothesis of this proposal is that changes in local protein synthesis in sensory axons alter the neuron's capacity for propagating noxious stimuli. The objective of this proposal is to understand how axonal transport and local protein synthesis contribute to hyperexcitability exhibited by damaged neurons leading to neuropathic pain states. We will use in vitro and in vivo methods to determine if the transport and sub-axonal localization of ion channel and neurotpeptide mRNAs are altered in neuropathic pain, and whether locally synthesized ion channels are functionally inserted into axoplasmic membranes and if this translation and trafficking are altered by neuropathic pain-associated stimuli. We will utilized chimeric mRNA reporter constructs to address axonal localization of these transcripts, both in cultured primary sensory neurons and in transgenic mice. GFP-tagged fusion proteins of locally synthesized ion channel proteins will be used to determine the functional relevance of axonally synthesized ion channels, with the ultimate goal of understanding how axonal trafficking and local synthesis of these proteins contributes to neuropathic pain. Neuropathic pain, the chronic pain experienced following injury, infection, or inflammation of peripheral nerves, sharply contrasts with normal pain, both is the molecular mechanisms which cause it and in their responses to conventional pain treatments. Current animal models of nerve trauma have provided some insights into the neuronal changes that occur in response to peripheral nerve damage - revealing a remarkable degree of plasticity in both the sensory neurons and spinal cord. Understanding how axonal transport and local protein synthesis contribute to increased hyperexcitability of these damaged sensory neurons may point to alternative methods of treating pathological pain states. [unreadable] [unreadable] [unreadable]
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0.904 |