raju shivarathri - medizinischen universität wien

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Raju SHIVARATHRI Medical University of Vienna Department of Medical Biochemistry Max F. Perutz Laboratories GmbH Dr. Bohr-Gasse 9/2, 1030 Vienna [email protected] Tel: +43-1-4277-61818 Research Group/Laboratory Prof. Dipl.-Ing. Dr. Karl Kuchler Current academic degree: M.Sc. Previous University: Osmania University, Hyderabad, India PhD thesis: Since 07/2014 Project title: Molecular mechanisms of chromatin modifications in Candida albicans-host interactions Project description: The increased incidence of invasive fungal infections has changed the landscape of fungal infections worldwide and greatly impacts healthcare management. Candida albicans is the most prevalent opportunistic human fungal pathogen and the leading cause of Candida blood-stream infections. Interactions of C. albicans with cells of the host immune system are usually complex and dynamic with each trying to gain an upper hand over the other. Dissecting the crucial molecular mechanisms in host and pathogen, how the host organizes the immune surveillance and how C. albicans circumvent the immune response in mammalian host is an exciting field. From the pathogen perspectives: in addition to the known pathogenicity mechanisms, epigenetic reprogramming has recently emerged as a prime mechanism critically determining the outcome of host-pathogen interactions. Thus, chromatin alterations may be one of the key survival strategies employed by fungal pathogen to escape from the host immune surveillance. Acetylation and deacetylation of chromatin constituents by histone acetyltransferases (HATs) and histone deacetylases (HDACs) are the two dynamic post-translational modifications modulating gene expression and pathogenicity. In fact, targeting HATs and HDACs could constitute a novel therapeutic approach to treat fungal infections. However, the molecular mechanisms of HATs and HDACs in fungal pathogenesis remain to be further explored. Hence, we are trying to understand the essential roles for HATs and HDACs in host-pathogen interactions.

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Page 1: Raju SHIVARATHRI - Medizinischen Universität Wien

Raju SHIVARATHRI

Medical University of Vienna Department of Medical Biochemistry Max F. Perutz Laboratories GmbH Dr. Bohr-Gasse 9/2, 1030 Vienna [email protected] Tel: +43-1-4277-61818

Research Group/Laboratory Prof. Dipl.-Ing. Dr. Karl Kuchler Current academic degree: M.Sc. Previous University: Osmania University, Hyderabad, India PhD thesis: Since 07/2014 Project title: Molecular mechanisms of chromatin modifications in

Candida albicans-host interactions

Project description: The increased incidence of invasive fungal infections has changed the landscape of fungal infections worldwide and greatly impacts healthcare management. Candida albicans is the most prevalent opportunistic human fungal pathogen and the leading cause of Candida blood-stream infections. Interactions of C. albicans with cells of the host immune system are usually complex and dynamic with each trying to gain an upper hand over the other. Dissecting the crucial molecular mechanisms in host and pathogen, how the host organizes the immune surveillance and how C. albicans circumvent the immune response in mammalian host is an exciting field. From the pathogen perspectives: in addition to the known pathogenicity mechanisms, epigenetic reprogramming has recently emerged as a prime mechanism critically determining the outcome of host-pathogen interactions. Thus, chromatin alterations may be one of the key survival strategies employed by fungal pathogen to escape from the host immune surveillance. Acetylation and deacetylation of chromatin constituents by histone acetyltransferases (HATs) and histone deacetylases (HDACs) are the two dynamic post-translational modifications modulating gene expression and pathogenicity. In fact, targeting HATs and HDACs could constitute a novel therapeutic approach to treat fungal infections. However, the molecular mechanisms of HATs and HDACs in fungal pathogenesis remain to be further explored. Hence, we are trying to understand the essential roles for HATs and HDACs in host-pathogen interactions.