The Administrative and Data Management Core (Core A) will provide a central resource for administering the program and will implement a management structure that will integrate and focus the scientific effort. This core will ensure scientific and fiscal oversight, facilitate communication and data exchange between investigators, and administer research funds. In the first specific aim, the Core will foster synergistic research efforts by implementing a LIMS based software systems to promote data capture, tracking, and analysis, enable web-based collaboration, and provide opportunities for planning and evaluation. The core will also foster communication between investigators by administering biweekly joint group meetings by conference call that also take advantage of a password-protected web site for data sharing. Core A will also organize and implement the annual retreat ofthe program, involving project leaders, principal researchers and members of the scientific advisory board. The second specific aim is to manage the scientific and fiscal components of the program. These components include implementation of a publication plan for collaborative projects and a plan to deal with material transfer and project overlap. Fiscal management of the program will be coordinated through the Grants and Administration Office (GAO) at the Salk Institute.
The Administrative and Data Management Core (Core A) will provide a central resource for administering this program which is aimed at gaining a comprehensive understanding ofthe innate immune response to HIV-1 infection. The function of the core will ensure the success of the project by implementing a management structure that will integrate and focus the scientific effort, establish scientific and fiscal oversight, facilitate communication and data exchange between investigators, and administer research funds. Successful completion of these projects will lead to the establishment of mathematical models that can explain and predict these innate immune responses, information that is important for future antiviral and vaccine approaches.
|Hansen, Maike M K; Desai, Ravi V; Simpson, Michael L et al. (2018) Cytoplasmic Amplification of Transcriptional Noise Generates Substantial Cell-to-Cell Variability. Cell Syst 7:384-397.e6|
|Jain, Prashant; Boso, Guney; Langer, Simon et al. (2018) Large-Scale Arrayed Analysis of Protein Degradation Reveals Cellular Targets for HIV-1 Vpu. Cell Rep 22:2493-2503|
|Hansen, Maike M K; Wen, Winnie Y; Ingerman, Elena et al. (2018) A Post-Transcriptional Feedback Mechanism for Noise Suppression and Fate Stabilization. Cell 173:1609-1621.e15|
|Alvarez, Raymond A; Maestre, Ana M; Law, Kenneth et al. (2017) Enhanced FCGR2A and FCGR3A signaling by HIV viremic controller IgG. JCI Insight 2:e88226|
|Park, Ryan J; Wang, Tim; Koundakjian, Dylan et al. (2017) A genome-wide CRISPR screen identifies a restricted set of HIV host dependency factors. Nat Genet 49:193-203|
|Ball, K Aurelia; Johnson, Jeffrey R; Lewinski, Mary K et al. (2016) Non-degradative Ubiquitination of Protein Kinases. PLoS Comput Biol 12:e1004898|
|Hultquist, Judd F; Schumann, Kathrin; Woo, Jonathan M et al. (2016) A Cas9 Ribonucleoprotein Platform for Functional Genetic Studies of HIV-Host Interactions in Primary Human T Cells. Cell Rep 17:1438-1452|
|Cheng, Zhang; Hoffmann, Alexander (2016) A stochastic spatio-temporal (SST) model to study cell-to-cell variability in HIV-1 infection. J Theor Biol 395:87-96|
|Guo, Haitao; König, Renate; Deng, Meng et al. (2016) NLRX1 Sequesters STING to Negatively Regulate the Interferon Response, Thereby Facilitating the Replication of HIV-1 and DNA Viruses. Cell Host Microbe 19:515-528|
|Heaton, Nicholas S; Moshkina, Natasha; Fenouil, Romain et al. (2016) Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection. Immunity 44:46-58|
Showing the most recent 10 out of 94 publications