The overall goal of the Systems Biology Core (Core B) is to provide experience, training and facilities for high-throughput measurements, together with expertise in bioinformatics and systems analysis in order to help the project investigators of the PPG to generate and test new hypotheses on systems-level mechanisms of short- and long-term hypoxia tolerance and susceptibility. Specifically, Core B will provide expertise and resources to: (a) acquire and analyze high-throughput data in humans, mice and flies on gene expression and genetic sequence variations in the context of hypoxia and the signaling pathways of interest; (b)acquire and analyze metabolic profiles and activity under normal and hypoxic conditions by NMR metabolomics, metabolic network reconstruction, and computational modeling;(c) to perform specific phenotypic measurements in flies and mice and develop computational models of physiological dynamics; and (d) deployment and curation of a physiological database and a web site and web-based tools for timely dissemination of data and findings. Core B will bring expertise in microarrays and pathway analysis, metabolic biochemistry and metabolomics, bioengineering and systems biology to work with all three projects and Core C in a variety of measurements and data analysis. In addition. Core B will be responsible for the web-based deployment and maintenance of data dissemination resources for the program project.
In the proposed PPG, the participating research projects will study adaptive mechanisms to hypoxia in cardiovascular and central nervous systems with the goal of identifying molecular signatures of hypoxia tolerance and susceptibility that will be relevant and useful clinically. The core will assist in these goals by providing systems biology tools and expertise to help the project to analyze gene expression, identify signaling pathways, determine molecular signatures and understand integrative mechanisms.
|Hartley, Paul S; Motamedchaboki, Khatereh; Bodmer, Rolf et al. (2016) SPARC-Dependent Cardiomyopathy in Drosophila. Circ Cardiovasc Genet 9:119-29|
|DÃaz-Trelles, RamÃ³n; Scimia, Maria Cecilia; Bushway, Paul et al. (2016) Notch-independent RBPJ controls angiogenesis in the adult heart. Nat Commun 7:12088|
|Gan, Zhuohui; Fu, Zhenxing; Stowe, Jennifer C et al. (2016) A Protocol to Collect Specific Mouse Skeletal Muscles for Metabolomics Studies. Methods Mol Biol 1375:169-79|
|Basaran, Kemal Erdem; Villongco, Michael; Ho, Baran et al. (2016) Ibuprofen Blunts Ventilatory Acclimatization to Sustained Hypoxia in Humans. PLoS One 11:e0146087|
|Azad, Priti; Zhao, Huiwen W; Cabrales, Pedro J et al. (2016) Senp1 drives hypoxia-induced polycythemia via GATA1 and Bcl-xL in subjects with Monge's disease. J Exp Med 213:2729-2744|
|Pamenter, Mathhew E; Powell, Frank L (2016) Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis. Compr Physiol 6:1345-85|
|Dewan, Sukriti; McCabe, Kimberly J; Regnier, Michael et al. (2016) Molecular Effects of cTnC DCM Mutations on Calcium Sensitivity and Myofilament Activation-An Integrated Multiscale Modeling Study. J Phys Chem B 120:8264-75|
|Stobdan, Tsering; Zhou, Dan; Ao-Ieong, Eilleen et al. (2015) Endothelin receptor B, a candidate gene from human studies at high altitude, improves cardiac tolerance to hypoxia in genetically engineered heterozygote mice. Proc Natl Acad Sci U S A 112:10425-30|
|GuimarÃ£es-Camboa, Nuno; Stowe, Jennifer; Aneas, Ivy et al. (2015) HIF1Î± Represses Cell Stress Pathways to Allow Proliferation of Hypoxic Fetal Cardiomyocytes. Dev Cell 33:507-21|
|Smith, Kimberly A; Voiriot, Guillaume; Tang, Haiyang et al. (2015) Notch Activation of Ca(2+) Signaling in the Development of Hypoxic Pulmonary Vasoconstriction and Pulmonary Hypertension. Am J Respir Cell Mol Biol 53:355-67|
Showing the most recent 10 out of 76 publications