2002-today Professor of Human Molecular Genetics at Department of Functional and Structural Biology and members of the PhD program in Genetics and Molecular Medicine.

Teaching:
Extensive experience of undergraduate and post-graduate teaching of genetics courses, and specialized state-of-art courses on Molecular Oncology and Cancer Genetics. Supervisor of more than 15 PhD students

Miscellanea:
- Member of the Administrative Council of Stazione Zoologica A. Dhorn Naples, (2002-2005).
- Research Fellow at International Institute of Genetics, CNR, Naples (1995-2001).
- Ad hoc referee for International journals:
Gene, J. Cellular Physiology, J. Cellular Biochemistry, Nucleic Acids Research, B.B.A., F.E.B.S. Letters, Cancer Research, Oncogene, EMBO J., EMBO Report.
- Ad hoc referee for 'Research and Fellowship Grants' of: Italian National Research Program in Biology; Italian Association for Cancer Research (AIRC); European Molecular Biology Organization, European Community; National Program on AIDS I.I.S. Rome.

Mammalian cells that sustain genotoxic as well as oncogenic insults must involve defensive mechanisms that either arrest cell cycle progression or trigger an apoptotic program. However, to discriminate between physiological and potentially harmful states, the defensive mechanisms must be finely tuned. A complex and non-redundant molecular pathways have been described to enable cells to respond to a plethora of stressful stimuli. Thus, a number of molecular responders are called in action when cells are subjected to scenarios that negatively affect their normal homeostasis. Because the RNA polymerase II transcription is the endpoint of signal transduction pathways that mediate the cellular response to different stimuli, it is not of a surprise that changes in the phosphorylatation state of the largest subunit of RNA polymerase II (RNAPII) mediated by the CDK9/CyclinT (P-TEFb) complex, occur in response to genotoxic insults. Accordingly, changes in the dynamic state, activity and stoichiometry of the P-TEFb complex are the hallmark of the cellular defensive mechanisms in response to a variety of genotoxic insults. Thus, P-TEFb is not only involved in controlling cell-cycle progression as specific co-factor of important cell growth controlling genes such as Myc and p53, but it also functions as an early sensor of genotoxic insults. The study on P-TEFb and the signaling pathways that regulate its activity is the major topic of research.

1. Amente S, Bertoni A, Morano A, Lania L, Avvedimento EV, Majello B (2010) LSD1-mediated demethylation of histone H3 lysine 4 triggers Myc-induced transcription. Oncogene 29: 3691-702.
2. Amente S, Lania L, Avvedimento EV, Majello B DNA oxidation drives Myc mediated transcription. (2010) Cell Cycle 9: 3002-4.
3. Napolitano G, Amente S, Castiglia V, Gargano B, Ruda V, Darzacq X et al (2010) Caffeine prevents transcription inhibition and P-TEFb/7SK dissociation following UV-induced DNA damage. PLoS One 5: e11245.
4. Amente, S., Gargano, B.,Napolitano, G., Lania, L. and Majello, B. (2009). Camptothein releases P-TEFb from the inactive 7SK snRNP complex. Cell Cylce 8, 1249-55
5. Gargano, B.,Fiorillo, M., Amente, S., Majello, B., and Lania, L. (2008). p14ARF is capable of promoting HIV-1 Tat degradation, Cell Cycle,7 1433-39.
6. Amente, S., Gargano, B., Diolaiti, D., Della Valle, G., Lania, L., and Majello, B. (2007). p14ARF interacts with N-Myc and inhibits its transcriptional activity. FEBS Lett 581, 821-825.
7. Gargano, B., Amente, S., Majello, B., and Lania, L. (2007). P-TEFb is a crucial co-factor for Myc transactivation. Cell Cycle 6, 2031-2037.
8. Napolitano, G., Varrone, F., Majello, B., and Lania, L. (2007). Activation of P-TEFb induces p21 leading to cell cycle arrest. Cell Cycle 6, 1126-1129.
9. Amente, S., Gargano, B., Varrone, F., Ruggiero, L., Dominguez-Sola, D., Lania, L., and Majello, B. (2006). p14ARF Directly Interacts with Myc Through the Myc BoxII Domain. Cancer Biol Ther 5.
10. Turano, M., Napolitano, G., Dulac, C., Majello, B., Bensaude, O., and Lania, L. (2006). Increased HEXIM1 expression during erythroleukemia and neuroblastoma cell differentiation. J Cell Physiol 206, 603-610.

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