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Kennet B. Marcu, Ph.D.

Photo (PhD, SUNY @ Stony Brook, 1975)
Professor Emeritus (as of January 1, 2016)
Department of Biochemistry and Cell Biology, Microbiology & Pathology Stony Brook University

University and Research Institute Affiliations/Memberships in Europe:

  • Biomedical Research Foundation Academy of Athens (BRFAA)
    • Basic Research Center
    • Genetics, Gene Therapy and Immunobiology Depts.
    • 4 Soranou Ephessiou Street  Athens, 115-27 Greece
  • IMBB-FORTH (Institute of Molecular Biology and Biotechnology of the Foundation for Research and Technology), Greece
  • Adjunct Professor, Univ. of Bologna
    • Senior Visiting Scientist
    • Laboratory of Immuno-Rheumatology and Tissue Regeneration/RAMSES
    • Rizzoli Orthopedic Research Institute
    • 40136 Bologna, Italy

USA Contact Information:
Biochemistry and Cell Biology Dept.
Life Sciences Rm. 330
Stony Brook University
Stony Brook, NY 11794-5215

Lab telephone: 631-632-8553
Fax: 631-632-9730

USA E-mail:
Europe E mail address:

Bologna, Italy Lab
Ioannina, Greece Lab

  • Research Description
    Research Projects (USA and Europe)

    As of January 1, 2016, I will be retiring from my full time Professorial position and thereafter will be Emeritus Professor at Stony Brook University. Thus as of January 1, 2016 I no longer have my own laboratory or research group at Stony Brook and will also no be an active member of any graduate programs (thus for these obvious reasons I can no longer take on students, technicians or postdoctoral fellows to work under my mentorship at Stony Brook University). However, in my retirement my research projects at Stony Brook University will be continuing in the laboratory of my collaborator Dr. Richard Kew in the Pathology Department; and I will also continue to give my block of lectures on B Lymphocyte development and function in immunity each September in Prof. Howard Fleit’s graduate immunology course (HBP 533) also in the Pathology Dept.  In my retirement I will be living in Bologna, Italy and will only be returning to the USA ~4 times each year, which are spread out ~2-4 months apart (each ~7-12 days in duration).  In addition, I will also continue to direct and co-direct basic biomedical research projects at other research institutes and Universities in the USA and Europe (where I also hold either Adjunct or Affiliated Appointments) on a year round basis including:  (1) The Hospital for Special Surgery in Manhattan, NY with my colleagues Drs. Miguel Otero, Kirsty Culley and Mary Goldring, and also in collaboration with Dr. Eleonora Olivotto at the Rizzoli Orthopedic Research Institute (affiliated with the University of Bologna in Bologna, Italy); (2) The IMBB-FORTH Biomedical Research Institute.  IMBB-FORTH (Ioannina Univ. Medical School, Ioannina, Greece) with my colleague Prof. Vagelis Kolettas; (3) The Biomedical Research Foundation Academy of Athens (BRFAA) in Athens. Greece with my colleagues Drs. Elia Chavdoula, Apostolos Klinakis and Dimitris Thanos; (4) San Diego State University’s Biology Dept with my colleague Prof. Roland Wolkowicz on the impact of NF-kappaB signaling in infectious viral disease.  Overall, my research will continue to involve the regulation and mechanisms of action of the inhibitor of NF-kB kinase (IKK) complex. The IKK signaling complex is essential for the activation of the NF-kB transcription factor family. Moreover, the IKKb and IKKa 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.  Thus IKKb and IKKa are orchestrators of developmental and inflammatory processes including all stress-like responses, innate and adaptive immunity and the survival and growth of normal and malignant cells. My research will continue to be focused on elucidating novel in vivomechanism(s) of action of IKKa and how IKKa’s functions collaborate with or differ from with those of its homologous partner kinase IKKb.  Together with colleagues and collaborators in the States and Europe I have been exploring the functional roles and mechanisms of action of IKKa and IKKb in different disease-related biological contexts including:  (1) novel cell migration responses specifically elicited in response to tissue sdamage initially invoking a pronounced inflammatory reaction that can eventually give way to tissue repair in part 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 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 cellular senescence and (4) specific alterations in cellular physiology that occur in cancer cell genesis and progression using a murine model of human lung cancer onset and progression.

    Other Link

    Osteoarthritic disease and Regenerative Medicine at the Rizzoli Research Institute (Bologna, Italy):
    NF-κΒ signaling in DNA damage & cellular senescence responses at the FORTH BRI (Ioannina, Greece)
    Europe E mail:

    -NF-kB signaling and impact in lung cancer development:

  • Publications
    • Valbuena, O.,   Marcu, K., Weigert M. and Perry, R.P. (1978). The Multiplicity of Germ Line Genes Specifying a Group of Related Mouse Kappa Chains With Implications for the Generation of Immunoglobulin Diversity.  Nature   276, 780-784
    • Schibler, U.,   Marcu, K. and Perry, R.P. (1978). The Synthesis and Processing of the Messenger RNAs Specifying Heavy and Light Chain Immunoglobulins in MPC-11 Cells.  Cell   l5, 1495-1509.
    • 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.
    • Tucker, P.,   Marcu, K.,  Slightom, J. and Blattner, F. (1979). Structure of the Constant and 3' Untranslated Regions of the Murine g2b Heavy Chain mRNA.  Science   206, 1299-1303.
    • Tucker, P.,   Marcu, K.,  Newell, N. Richards, J. and Blattner, F. (1979). Sequence of the Cloned Gene for the Constant Region of Murine g2b Immunoglobulin Heavy Chain. Science   206, 1303-1306.
    • 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., Lang, R.B., Stanton, L.W. and Harris, L.J. (1982). A Model for the Molecular Requirements of Immunoglobulin Heavy Chain Class Switching.  Nature   298, 87 89.
    • Marcu, K.B. and Cooper, M. (1982). New Views of the Immunoglobulin Heavy-chain Switch.  Nature   298, 327-328.
    • Marcu, K.B. (1982). Immunoglobulin Heavy Chain Constant Region Genes.  Cell   29, 719-721.
    • 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.
    • Stanton, L.W., Fahrlander, P.D., Tesser, P.C. and   Marcu, K.B. (1984). Nucleotide Sequence Comparison of Normal and Translocated Murine c-myc Genes.  Nature   310, 423-425.
    • 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., Fahrlander, P.D., Yang, J.Q. and   Marcu, K.B. (1985). Amplification and Altered Expression of the c-myc Oncogene in A-MuLV Transformed Fibroblasts. Nature   317, 440-443.
    • Fahrlander, P.D., Piechaczyk, M. and   Marcu, K.B.  (1985). Chromatin Structure of the Murine c-myc Locus: Implications for the Regulation of Normal and Chromosomally Translocated Genes.  EMBO J.   4, 3195-3202.
    • Nepveu, A. and   Marcu, K.B. (1986). Intragenic Pausing and Anti-sense Transcription Within the Murine c-myc Locus.  EMBO J.   5, 2859-2865.                                                      
    • Ott, D.E., Alt, F.W. and   Marcu, K.B.  (1987). Immunoglobulin Heavy Chain Switch Region Recombination Within a Retroviral Vector in Murine pre-B Cells.  EMBO J.   6, 577-584. 
    • Bossone, S.A., Asselin, C., Patel, A.J. and   Marcu, K.B. (1992). MAZ, a Novel Zinc Finger Protein Binds to c-myc and C2 Gene Sequences Regulating Transcriptional Initiation and Termination.  Proc. Natl. Acad. Sci. USA   89, 7452-7456. 
    • Marcu, K.B., Bossone, S.A. and Patel, A.J. (1992). MYC Regulation and Function.  Ann. Rev. Biochem.   61, 809-860. 
    • Ballantyne, J., Henry, D.L., Briere, F., Mueller, J., Kehry, M., Snapper, C. and   Marcu, K.B.  (1998) Efficient recombination of a switch substrate retrovector in CD40 activated B lymphocytes: Implications for the regulation of the IgCH switch-recombinase. J. Immunol. 161, 1336-1347. 
    • McKenzie, F.R., Connelly, M.A., Balzarano, D., Müller, J.R., Geleziunas, R. and   Marcu, K.B.  (2000) Functional isoforms of IKKa (IkB-kinase-a) lacking leucine zipper and helix-loop-helix domains reveal that IKKa and IKKb have different activation requirements. Mol. Cell. Biol. 20: 2635-2649. 
    •  Li, J., Peet, G.W., Balzarano, D., Li, X., Massa, P., Barton, R. and   Marcu, K.B.  (2001) Novel NEMO/IKKg and NF-kB target genes at the pre-B to immature B cell transition. J. Biol. Chem. 276: 18579-18590. 
    •  Li, X., Massa, P., Hanidu, A., Peet, G.W., Aro, P., Savitt, A., Mische, S. Li, J. and   Marcu, K.B.  (2002) IKKa, IKKb and NEMO/IKKg are each required for the NF-kB mediated inflammatory response program. J. Biol. Chem. 277: 45129-45140. 
    • Massa, P.E., Li, X., Hanidu, A., Siamas, J., Pariali, M., Pareja, J., Savitt, A.G., Catron,   K.M., Li, J., and   Marcu, K.B. (2005). Gene expression profiling in conjunction with physiological rescues of IKKa null cells with Wt. or mutant IKKa reveals distinct classes of IKKa/NF-kB dependent genes. J. Biol. Chem. 280:  14057-14069 
    • Palumbo, R., Glavez, B.G., Pusterla, T., De Marchis, F., Cossu, G.,   Marcu, K.B. and Bianchi, M.E. (2007). Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kB activation. J. Cell Biol. 179:  33-40 
    • Sansone, P., Storci, G-L., Tavolari, S.,Guarnieri, T., Giovannini, C., Taffurelli, M., Ceccarelli, C., Santini, D., Paterini, P.,   Marcu, K.B., Chieco ,   P., and Bonafe, M. (2007). Interleukin-6 triggers malignant features in mammospheres from human ductal breast carcinoma and normal mammary gland.  J. Clinical Investigation 117: 3988-4002. 
    • 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 IKKa and IKKb in the differentiation of primary human osteoarthritic chondrocytes.  Arthritis and Rheumatism 58: 227-239. 
    • Penzo, M., Massa, P.E., Olivotto, Bianchi. F., Borzi, R.M., Hanidu, A., Li, X., Li. J. and    Marcu, K.B.  (2009).   Sustained NF-kB activation produces a short-term cell proliferation block in conjunction with repressing effectors of cell cycle progression controlled by E2F or FoxM1. J. Cellular Physiology 218: 215-227.  
    • Batsi. C., Markopoulou, S., Kontargiris, E., Charalambous, C. Thomas, C., Christoforidis, S., Kanavaros, P.  Constantinou, A.I.,   Marcu ,   K.B . and Kolettas, E. (2009). Bcl-2 blocks 2-methoxyestradiol induced leukemia cell apoptosis by a p27Kip1-dependent G1/S cell cycle arrest in conjunction with NF-kB.  Biochemical Pharmacology 78: 33-44.
    • Batsi, C., Markopoulou, A., Vartholomatos, G., Georgiou, I., Kanavaros, P., Gorgoulis, V.C.,   Marcu, K.B. and Kolettas, K. 2009. Chronic NF-kB activation delays RasV12-induced premature senescence of human fibroblasts by suppressing the DNA damage checkpoint response. Mechanisms of Aging and Development 130: 409-419. 
    • Marcu, KB, Otero, M., Olivotto, E., Borzi, R-M. and Goldring, M.B. (2010). NF-kB Signaling:  Multiple angles to target OA. In Innovative Drug Targets for Osteoarthritis Therapy. Current Drug Targets 11 (5): 599-613. 
    • 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. 
    • Borzi, R-M., Olivotto, E., Pagani, S., Vitellozzi, R., Neri, S., Battistelli, M., Falcieri, E., Facchini, A., Flamigni, F., Penzo, M., Platano, D., Santi, S., Facchini, A. and   Marcu, K. B. 2010. Matrix metalloproteinase 13 loss associated with impaired ECM remodeling disrupts chondrocyte differentiation by concerted effects on multiple regulatory factors. Arthristis and Rheumatism 62: 2370-2381. 
    • Storci, G., Sansone, P., Mari, S., D’Uva, G., Tavolari, S., Guarnirei, T., Taffurellli, M.,   
    • Ceccarelli, C., Santini, D., Cheico, P.,   Marcu, K.B., Bonafe, M. 2010. TNFa up-regulates  SLUG via the NF-kB/HIF1alpha axis, which imparts breast cancer cells with a stem cell-like phenotype. J. Cell Physiol. 225:  682-691. 
    • Goldring, M.B., Otero ,   M., Plumb, D.A., Dragomir, C., Favero, M., El Hachem, K., Hashimoto, K.,  Roach, H.I., Olivotto, E., Borzi, R-M.,  and   Marcu, K.B.  2011. Roles of Inflammatory and anabolic cytokines in cartilage cytokine in cartilage metabolism: signals and multiple effectors converge upon MMP-13 regulation in osteoarthritis.  European Cells and Materials Journal 21:  202-220.
    • Goldring, M.B. and   Marcu, K.B. 2012. Epigenomic and microRNA-mediated regulation  
    • in cartilage development, homeostasis, and osteoarthritis.  Trends in Molecular Medicine  18(2): 109-118
    •  Kew, R.R., Penzo. M., Habiel, D. M. and   Marcu, K. B. 2012. The IKKa-dependent NF-kB 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.   PMCID:   PMC3288724  
    • Sfikasa, A., C. Batsia, E. Tselikoua, G. Vartholomatosc, N. Monokrousosd, P. Pappase, S. Christoforidisf, T. Tzavarash, P. Kanavarosb, V.G. Gorgoulisi,   K.B. Marcu , and E. Kolettas. 2012. The canonical NF-κB pathway differentially protects normal and human tumor cells from ROS-induced DNA damage. Cellular Signaling 24 (11): 2007-2023.   PMCID: PMC3432746.
    •  Samaniego S,   Marcu KB  (2013) IKKβ in Myeloid Cells Controls the Host  Response to  
    •  Lethal and Sublethal   Francisella tularensis  LVS Infection. PLoS ONE  8(1): e54124.   doi:10.1371/journal.pone.0054124. 
    • Olivotto, E., Miguel Otero, M., Astolfi, A. Platano, D., Facchini, A. Pagani, S., Flamigni, F., Facchini, A., Goldring, M.B., Borz ì, 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.   
    • Penzo, M,, Habiel, D.M., Ramadass, M., Kew, R. R. and Marcu, K.B. (2014). Cell migration to CXCL12 reuires simultaneous IKKa and IKKb-dependent NF-kB signaling.  BBA-Mol.Cell Res. 1843 (9): 1796-1804. 
    • Olivotto, E., Otero ,   M., Marcu ,   KB and Goldring ,   MB (2015). Pathophysiology of  Osteoarthritis: Canonical NF-kappaB/IKKbeta-dependent and kinase independent effects of IKKalpha in Cartilage Degradation and Chondrocyte Differentiation.  RMD Open 1:e000061.doi:10.1136/rmdopen-  
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