Kenneth B. Marcu, Ph.D. Professor Department of Biochemistry and Cell Biology, Microbiology & Pathology Stony Brook University And Senior Scientist (and Adjunct Professor, Univ. of Bologna) Immunologia e Genetica Dept. Istituti Ortopedia Rizzoli Bologna, Italy USA Contact Information: Biochemistry and Cell Biology Dept. Life Sciences Rm. 326 and 330 Stony Brook University Stony Brook, NY 11794-5215 Lab telephone: 631-632-8553 Fax: 631-632-9730 E-mail: kenneth.marcu@stonybrook.edu
Other Links		Osteoarthritic disease and Regenerative Medicine at the Rizzoli Research Institute (Bologna, Italy): http://www.ior.it/immunologia NF-κΒ signaling in DNA damage & cellular senescence responses at the FORTH BRI (Ioannina, Greece) Europe E mail: kenneth.marcu@unibo.it
Research Description

My research projects are ongoing concurrently in the United States and Europe. I direct and codirect multiple research projects at Stony Brook University and several other research institutions on a year round basis with Stony Brook University representing my principle, institutional base. I travel about a lot on a year round basis to maintain my multiple research projects and other scholarly pursuits. In addition to my research activities at Stony Brook, I have several other projects on-going at the Rizzoli Orthopedic Research Institute in Bologna, Italy and the FORTH BRI at the Ioannina Medical School, Ioannina, Greece. My research activities (ca December 2011) concern the regulation and mechanisms of action of the inhibitor of NF-κB kinase (IKK) complex. The IKK signaling complex is essential for the activation of the NF-κB transcription factor family, which regulate stress-like responses, innate and adaptive immunity and the survival and growth of normal and malignant cells. Moreover, the IKKβ and IKKα serine threonine kinases in the IKK signalsome also functionally impact on a number of other NF-kB independent growth and differentiation pathways in various cell types. The central focus of my research is to elucidate novel in vivo mechanism(s) of action of IKKα and how IKKα’s functions collaborate with or differ from with those of its NF-κΒ activating partner kinase IKKβ. Together with colleagues and collaborators in the States (Stony Brook University, Hospital for Special Surgery, Manhattan, NY and Biological Sciences Dept, San Diego State University, San Diego, CA, Harvard Medical School, Boston, MA) and Europe (Rizzoli Research Institute, the University of Bologna, Bologna, Italy, and the BRI-FORTH Institute, University of Ioannina Medical School, Ioannina, Greece), I am exploring the functional roles and mechanisms of action of IKKα and IKKβ in different disease-related biological settings including: (1) novel cell migration responses specifically elicited in response to tissue damage initially invoking a pronounced inflammatory reaction that can eventually give way to tissue repair via the recruitment of progenitor, stem cells, (2) gene expression and epigenomic regulation associated with the maintenance of articular chondrocyte homeostasis and/or differentiation programming and mechanical and pro-inflammatory stress culminating in osteoarthritic disease in novel IKK deleter inducible mice, (3) alterations in gene expression programming in response to specific forms of extracellular stress leading to DNA damage and repair and premature cellular senescence and (4) specific alterations in cellular physiology that occur in cancer cell genesis and progression associated with an epithelial to mesenchymal cell transition and hypoxic environments invoking IKK/NF-κΒ-dependent stress-like reactions in novel murine models and primary human cells.

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