Biomedical Ίδρυμα Ιατροβιολογικών Ερευνών, Ακαδημίας ΑθηνώνΑκαδημία Αθηνών
Επιστημονικό Προσωπικό

Kenneth Kenneth Marcu, PhD
Επιστημονικός Συνεργάης

Τηλέφωνο : +30 210 6597 069
e-mail :

Κέντρο :

Βασική Έρευνα

Σύντομο Βιογραφικό

Dr. Marcu directs or co-directs research projects at several different institutions in the USA and Europe including: Stony Brook University, Stony Brook, NY, the Hospital for Special Surgery in Manhattan, NY, the Rizzoli Orthopedic Research Institute (affiliated with the University of Bologna in Bologna, Italy), the IMBB-FORTH Biomedical Research Institute based at Ioannina University (in collaboration with Prof. Evangelos Kolettas) and with several groups at the BRFAA in Athens, Greece (e.g., Drs. Apostolos Klinakis, Evangelos Andreakos and Apostolos Klinakis).  His research projects involve the regulation and mechanisms of action of the inhibitor of NF-B kinase (IKK) complex. The IKK signaling complex is essential for the activation of the NF-B transcription factor family, which regulate stress-like responses, innate and adaptive immunity and the survival and growth of normal and malignant cells.  Moreover, the IKK and IKK serine threonine kinases in the IKK signalsome also functionally impact on a number of other NF-B independent growth and differentiation pathways in various cell types. His current research is focused on elucidating novel in vivo mechanism(s) of action of IKK and how IKK’s functions collaborate with or differ from with those of its NF-B activating partner kinase IKK.  Together with his colleagues collaborators in the States and Europe he is exploring the functional roles and mechanisms of action of IKK and IKK in different disease-related biological contexts 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, differentiation programming and mechanical and pro-inflammatory stress that can lead to osteoarthritic disease; (3) alterations in gene expression programming in response to specific forms of extracellular stress including pro-inflammatory oncogenic events leading to DNA damage and premature cell aging (cellular senescence) and (4) specific alterations in gene expression programming cellular physiology associated with the onset and progression of lung cancer.

Επιλεγμένες Δημοσιεύσεις

Marcu, K.B., Schibler, U. and Perry, R.P. (1979). The Nuclear Transcripts of Mouse Heavy Chain Immunoglobulin Contain Only the Expressed Class of C-region Sequences.  Science 241, 1087-1088.

Marcu, K.B., Banerji, J., Penncavage, N., Lang, R. and Arnheim, N. (1980). The 5' Flanking Region of Immunoglobulin Heavy Chain Constant Region Genes Displays Length Heterogeneity in the Germ Lines of Inbred Mouse Strains.  Cell 22, 187-196.

Harris, L.J., Lang, R.B. and Marcu, K.B. (1982). Non-immunoglobulin Associated DNA Rearrangements in Mouse Plasmacytomas.  Proc. Natl. Acad. Sci. USA 79, 4175-4179.

Marcu, K.B., Harris, L.J., Stanton, L.W., Erikson, Watt, J. R. and Croce, C.M. (1983). Transcriptionally Active c-myc Oncogene is Contained Within NIARD, a DNA Sequence Associated With Chromosome Translocations in B Cell Neoplasia.  Proc. Natl. Acad. Sci.  USA 80, 519-523.

Stanton, L.W., Watt, R. and Marcu, K.B. (1983). Translocation, Breakage and Truncated Transcripts of the c-myc Oncogene in Murine Plasmacytomas.  Nature 303, 401-406.

Piechaczyk, M., Yang, J.Q., Blanchard, J., Jeanteur, Ph. and Marcu, K.B. (1985). Post-Transcriptional Mechanisms are Responsible for
Accumulation of Truncated c-myc RNAs in Murine Plasma Cell Tumors.  Cell 42, 589-597.

Nepveu, A. and Marcu, K.B. (1986). Intragenic Pausing and Anti-sense Transcription Within the Murine c-myc Locus.  EMBO J. 5, 2859-2865.

Li, X., Massa, P., Hanidu, A., Peet, G.W., Aro, P., Savitt, A., Mische, S. Li, J. and  Marcu, K.B. (2002) IKKα, IKKβ and NEMO/IKKγ are each required for the NF-B mediated inflammatory response program. J. Biol. Chem. 277: 45129-45140.

Olivotto, E., Borzi', R.M., Vitellozzi, R., Pagani, S., Facchini, A., Battistelli, M., Penzo, M., Li, X., Flamigni, F., Li, J., Falcieri, E., Facchini, A.,  and Marcu, K.B. (2008) Differential requirements for IKKα and IKKβ in the differentiation of primary human osteoarthritic chondrocytes.  Arthritis and Rheumatism 58: 227-239.

Penzo, M., Molteni, R., Suda, T., Samaniego, S., Raucci, A., Habiel, D.M., Miller, F., Jiang, H-P., Li, J.., Pardi, R., Palumbo, R., Olivotto, E., Kew, R.R., Bianchi, M. and Marcu, K.B. (2010). Inhibitor of NF-{kappa}B Kinases {alpha} and {beta} are both essential for High Mobility Group Box 1-mediated chemotaxis. J. of Immunol 184 (8): 4497-4509.

Kew, R.R., Penzo. M., Habiel, D. M. and Marcu, K. B. (2012) The -dependent NF-B p52/RelB non-canonical pathway is essential to sustain a CXCL12 autocrine loop in cells migrating in response to HMGB1. Journal of Immunology 188 (5): 2380-2386.

Olivotto, E., Miguel Otero, M., Astolfi, A. Platano, D., Facchini, A. Pagani, S., Flamigni, F., Facchini, A., Goldring, M.B., Borzì, R.M., and Marcu, K.B. (2013). IKKalpha/CHUK regulates extracellular matrix remodeling independent of its kinase activity to facilitate articular chondrocyte differentiation. PLOS ONE 8(9): e73024.


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