BASIC SCIENCE I CORE: CELL CULTURE/NEUROTROPIC VIRUS, NEUROSCIENCE, AND PROTEOMICS The overall objective of the Basic Science Core I (BSCI) is to provide in vitro shared resources and training to basic and clinical researchers to study neurological disorders at the molecular level, related to Human Immunodeficiency Virus (HIV) infection. During HIV central nervous system (CNS) disease, disparities between virus-associated insults and host-mediated attempts at rescue and repair are responsible for cognitive deficits. To protect cells of the CNS, and to promote beneficial responses, key elements in the signaling crosstalk between cells of the CNS and virus must be understood. Information regarding cell-virus biochemical signaling interactions must be addressed, in large part, by in vitro studies. The BSCI will provide investigators with reliable access to high quality CNS cell cultures, virus and viral products, and other factors that contribute to HIV CNS disease which are critical to delineate signaling pathways important in disease progression. BSCI will also provide assistance and expertise in classical neuroscience techniques and tools to support investigation of cellular/molecular interactions between cells of the CNS and HIV that underlie neurocognitive dysfunction. The BSCI will also provide state-of-the-art services for discovering the molecular mechanisms involved in the development of AIDS-associated CNS dysfunction through proteomics and data analysis. Novel methods for discovering of biomarkers, innovative differential expression profiling and bioinformatics along with interactomics and phosphoproteomics are among the services that will be reliably and efficiently offered to the investigators. Our core will work closely with the other cores to promote a comprehensive multidisciplinary collaborative center program. This synergistic approach will ensure the success of both recipients of CNACC developmental awards and other members of the Center in conducting productive high impact research into HIV associated neurological disorders.
This core will provide cell culture and virology services to investigators performing biomedical research on AIDS and the nervous system. Moreover, in the context of this core facility, neuroAIDS researchers will be able to analyze clinical samples, cell culture, or animal models for biomarkers of disease and to uncover mechansims involved in the development and progression of CNS disorders associated with HIV-1 infection.
|Mohseni Ahooyi, Taha; Shekarabi, Masoud; Decoppet, Emilie A et al. (2018) Network analysis of hippocampal neurons by microelectrode array in the presence of HIV-1 Tat and cocaine. J Cell Physiol 233:9299-9311|
|Tahrir, Farzaneh G; Shanmughapriya, Santhanam; Ahooyi, Taha Mohseni et al. (2018) Dysregulation of mitochondrial bioenergetics and quality control by HIV-1 Tat in cardiomyocytes. J Cell Physiol 233:748-758|
|Donadoni, Martina; Sariyer, Rahsan; Wollebo, Hassen et al. (2018) Viral tumor antigen expression is no longer required in radiation-resistant subpopulation of JCV induced mouse medulloblastoma cells. Genes Cancer 9:130-141|
|Cotto, Bianca; Natarajaseenivasan, Kalimuthusamy; Ferrero, Kimberly et al. (2018) Cocaine and HIV-1 Tat disrupt cholesterol homeostasis in astrocytes: Implications for HIV-associated neurocognitive disorders in cocaine user patients. Glia 66:889-902|
|Bella, Ramona; Kaminski, Rafal; Mancuso, Pietro et al. (2018) Removal of HIV DNA by CRISPR from Patient Blood Engrafts in Humanized Mice. Mol Ther Nucleic Acids 12:275-282|
|Mohseni Ahooyi, Taha; Shekarabi, Masoud; Torkzaban, Bahareh et al. (2018) Dysregulation of Neuronal Cholesterol Homeostasis upon Exposure to HIV-1 Tat and Cocaine Revealed by RNA-Sequencing. Sci Rep 8:16300|
|Craigie, Michael; Cicalese, Stephanie; Sariyer, Ilker Kudret (2018) Neuroimmune Regulation of JC Virus by Intracellular and Extracellular Agnoprotein. J Neuroimmune Pharmacol 13:126-142|
|Mele, Anthony R; Marino, Jamie; Chen, Kenneth et al. (2018) Defining the molecular mechanisms of HIV-1 Tat secretion: PtdIns(4,5)P2 at the epicenter. Traffic :|
|Delcour, Maxime; Russier, Michaël; Castets, Francis et al. (2018) Early movement restriction leads to maladaptive plasticity in the sensorimotor cortex and to movement disorders. Sci Rep 8:16328|
|Cotto, Bianca; Li, Hongbo; Tuma, Ronald F et al. (2018) Cocaine-mediated activation of microglia and microglial MeCP2 and BDNF production. Neurobiol Dis 117:28-41|
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