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dc.contributorNot Applicableen_US
dc.contributor.authorPANEPINTO, JOHN C Principal Investigatoren_US
dc.date30-Jun-11en_US
dc.date2009en_US
dc.date.accessioned2011-04-18T20:56:59Zen_US
dc.date.accessioned2011-04-19T18:30:38Z
dc.date.available1-Jul-08en_US
dc.date.available2011-04-18T20:56:59Zen_US
dc.date.available2011-04-19T18:30:38Z
dc.date.issued2011-04-18T20:56:59Zen_US
dc.identifier7626396en_US
dc.identifier5K22AI070647-02en_US
dc.identifier70647en_US
dc.identifier.urihttp://hdl.handle.net/10477/979
dc.descriptionAfrica;Aminoglycoside Antibiotics;Antifungal Agents;antiretroviral therapy;Area;Attenuated;biological adaptation to stress;Biological Assay;Boxing;Brain;c-myc Genes;Candidate Disease Gene;career;Cell Cycle;Cell Cycle Progression;Cell Cycle Regulation;Cell physiology;Cellular Immunity;Characteristics;Chimeric Proteins;Communities;Cryptococcus;Cryptococcus neoformans;Cryptococcus neoformans infection;Data;Defect;design;Disease;DNA Damage;DNA Repair Gene;Drug Delivery Systems;Encephalitis;Environment;ERCC3 gene;Exhibits;fitness;Flucytosine;Fluorouracil;Framycetin Sulfate;fungus;Future;Goals;Growth;Harvest;HIV;Human;human disease;hydroxyurea;Immune;Infection;insight;Investigation;Kinetics;Lead;Life;Lung;macrophage;Maintenance;Measurement;Measures;Meningitis;Messenger RNA;Microarray Analysis;Modeling;Morbidity - disease rate;Mortality Vital Statistics;mRNA decapping;mRNA Stability;mRNA Transcript Degradation;Mus;mutant;Mutation;new therapeutic target;Northern Blotting;novel;Nutrient;Organism;overexpression;Oxidative Stress;pandemic disease;pathogen;Pathogenesis;Pathogenicity;Pathway interactions;Patients;Phagosomes;Pharmaceutical Preparations;Phenanthrolines;Phenotype;Plague;Ploidies;Predisposition;Process;Processed Genes;programs;Proliferating;Proteins;reconstitution;Regulation;Regulator Genes;Research;Research Personnel;Research Proposals;research study;response;RNA Helicase;RNA Interference;Role;Signal Transduction;Site;Southeastern Asia;Starvation;Stress;stress tolerance;Syndrome;Systemic infection;Temperature;Testing;Time;tool;trait;Transcript;Up-Regulation (Physiology);Virulence;Work;en_US
dc.descriptionAmount: $ 107443en_US
dc.description.abstractDESCRIPTION (provided by applicant): Cryptococcus neoformans is a major cause of morbidity and mortality in patients with defects in cell mediated immunity. This research proposal sets out to investigate the role of regulated mRNA degradation in the ability of C. neoformans to survive within the host and cause disease. The overall hypothesis is that Ccr4, the catalytic component of the mRNA degradation machinery is an important regulator of thermotolerance and pathogenic fitness. The first aim sets out to assess the effect of Ccr4 deletion on thermotolerance, pathogenicity and mRNA degradation. Aim 2 will determine the role of Ccr4 in cell cycle regulation and response to replication stress under conditions that mimic conditions in the host including growth within macrophages. The third aim sets out to identify conditions that promote colocalization of Ccr4 with another regulator of pathogenic fitness, Vad1, in processing bodies, the site of mRNA degradation. This will identify conditions under which Vad1 and Ccr4 function coordinately and independently in response to stress. Ccr4 is a potential drug target, as deletion results in a severe growth defect at host temperature. This identification of cellular processes and genes regulated through this pathway has the potential for identification of novel therapeutic targets, and will provide insight into how C. neoformans is able to adapt to the stressful environment of the host and cause human disease.en_US
dc.titleCCR4 IN THE MAINTENANCE OF THERMOTOLERANCE AND PATHOGENICITY OF C. NEOFORMANSen_US
dc.typeNIH Grant Awarden_US


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