The Administrative Core (Core A) provides centralized services that support the Principal Investigator, Project Leaders, and Core Resource Directors of the Program Project, and is responsible for continuity, coordination and oversight of the projects and support cores of the Program Project. The primary functions of the Core include the following: (a) provide direction and overall management of the Program;(b) foster communication and integration of the research projects and the cores by conducting regular scientific meetings of PPG investigators;(c) oversee and coordinate the efforts of the support cores by oversight committees and monitoring efficient usage;(d) monitor and track all expenditures of the PPG and ensure accurate allocation of funds;(e) provide logistics support for other aspects including personnel actions, IACUC documents, record keeping, progress reports;(f) arrange and coordinate meetings of the PPG internal and external scientific advisory boards, including travel. These Advisory groups will review progress of the entire Program, provide advice, and evaluate each project on at least a yearly basis. In addition, the Core will provide coordination and continuity to each of the projects and cores for the duration of the PPG. Stuart A. Aaronson, MD, will direct the Core with Ed Hicks, MBA, providing administrative and operational oversight. Ms. Donna Chiodi will provide general administrative assistance to all program project participants. The Core will operate out of the administrative suite of the Department of Oncological Sciences.
The overall relevance of this research Program is that major insights gained in the investigation of cellular stress responses involving p53 and understanding of the complex regulatory networks in which p53 acts offer the potential for improved therapeutic approaches to cancers as well as to other pathophysiologic conditions, which activate this central mediator of cell fate decisions.
|Mungamuri, S K; Wang, S; Manfredi, J J et al. (2015) Ash2L enables P53-dependent apoptosis by favoring stable transcription pre-initiation complex formation on its pro-apoptotic target promoters. Oncogene 34:2461-70|
|Hager, Kayla M; Gu, Wei (2014) Understanding the non-canonical pathways involved in p53-mediated tumor suppression. Carcinogenesis 35:740-6|
|Wang, Shang-Jui; Gu, Wei (2014) To be, or not to be: functional dilemma of p53 metabolic regulation. Curr Opin Oncol 26:78-85|
|Smith, Steven G; Sanchez, Roberto; Zhou, Ming-Ming (2014) Privileged diazepine compounds and their emergence as bromodomain inhibitors. Chem Biol 21:573-83|
|Mungamuri, Sathish Kumar; Murk, William; Grumolato, Luca et al. (2013) Chromatin modifications sequentially enhance ErbB2 expression in ErbB2-positive breast cancers. Cell Rep 5:302-13|
|Kracikova, M; Akiri, G; George, A et al. (2013) A threshold mechanism mediates p53 cell fate decision between growth arrest and apoptosis. Cell Death Differ 20:576-88|
|Senturk, Emir; Manfredi, James J (2013) p53 and cell cycle effects after DNA damage. Methods Mol Biol 962:49-61|
|Hamard, Pierre-Jacques; Barthelery, Nicolas; Hogstad, Brandon et al. (2013) The C terminus of p53 regulates gene expression by multiple mechanisms in a target- and tissue-specific manner in vivo. Genes Dev 27:1868-85|
|Chen, Delin; Kon, Ning; Zhong, Jiayun et al. (2013) Differential effects on ARF stability by normal versus oncogenic levels of c-Myc expression. Mol Cell 51:46-56|
|Namba, Takushi; Tian, Fang; Chu, Kiki et al. (2013) CDIP1-BAP31 complex transduces apoptotic signals from endoplasmic reticulum to mitochondria under endoplasmic reticulum stress. Cell Rep 5:331-9|
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