B.S. 1990, Rutgers University, New Brunswick, NJ
Ph.D. 1997, University of Pennsylvania School of Medicine, Philadelphia, PA
Post-doc, 2000, University of California, San Francisco School of Medicine
Ph.D., 1997, University of Pennsylvania School of Medicine, Molecular Virology B.S., 1990, Rutgers University
Gonzalez-Lopez, O, DeCotiis, J, Goyeneche, C, Mello, H, Vicente-Ortiz, BA, Shin, HJ,
Driscoll, KE, Du, P, Palmeri, D, and
Lukac, DM (2019). A herpesvirus transactivator and cellular POU proteins extensively
regulate DNA binding of the host
Notch signaling protein RBP-Jk to the virus genome. Journal of Biological Chemistry 294:
DeCotiis, JL, NC Ortiz, BA Vega, and DM Lukac. "An easily transfectable cell line that
produces an infectious
reporter virus for routine and robust quantitation of Kaposi's sarcoma-associated
herpesvirus reactivation." J.
Virol Methods 247: 99-106. (2017)
DeCotiis, JL, and DM Lukac. KSHV and the Role of Notch Receptor Dysregulation in Disease
Pathogens 4: 6 (2017)
Guito, J.; Lukac, D.M. (2015) KSHV Reactivation and Novel Implications of Protein
Isomerization on Lytic Switch
Control. Viruses 7: 72-109. http://www.mdpi.com/1999-4915/7/1/72
Guito, J, A Gavina, D Palmeri, and DM Lukac (2014). The cellular peptidyl-prolyl
Pin1 regulates reactivation of Kaposi's sarcoma-associated herpesvirus from latency. J
Shin, HJ, DeCotiis, J, Giron, M, Palmeri, D and DM Lukac. (2014), "Histone Deacetylase
Classes I and
II Regulate Kaposi's Sarcoma-Associated Herpesvirus Reactivation." J Virol 88:1281-1292.
Guito, J, DM Lukac Kaposi's sarcoma-associated herpesvirus Rta Promoter Specification and
(Invited Review) Frontiers in Microbiology 3:30. (2012).
Palmeri, D, Carroll, KD, Gonzalez-Lopez, O, and DM Lukac. Kaposi's sarcoma-associated
tetramers make high affinity interactions with repetitive DNA elements in the Mta promoter
to stimulate DNA
binding of RBP-Jk/CSL. Journal of Virology 85: 11901-11915. (2011).
Spadavecchia, S., Gonzalez-Lopez, O., Carroll KD, Palmeri, D, and DM Lukac Convergence of
Associated Herpesvirus Reactivation with Epstein-Barr Virus Latency and Cellular Growth
Mediated by the Notch
Signaling Pathway in Coinfected Cells , Journal of Virology 84: 10488-10500. (2010).
Bu, W, D Palmeri, R Krishnan, R Marin, VM Aris, P Soteropoulos, and DM Lukac.
Identification of Direct
Transcriptional Targets of the Kaposi's sarcoma-associated herpesvirus (KSHV) Rta Lytic
Switch Protein by
conditional nuclear localization of Rta. Journal of Virology 82: 10709-10723. (2008).
Host-virus interactions in oncogenic herpesviral infection
Kaposi's Sarcoma-Associated Herpesvirus (KSHV; also known as Human herpesvirus-8) is a DNA tumor virus that is the etiologic agent of Kaposi's Sarcoma and other AIDS-related cancers. Epidemiologic studies have demonstrated that lytic reactivation of KSHV from latency is required for progression of these unique cancers. We are studying the critical host-virus interactions, at the molecular level, that govern reactivation of the virus, in order to gain a thorough understanding of the pathogenesis of KSHV infection.
We have previously demonstrated that a single viral protein, called Rta (for "replication and transcriptional activator"), functions as a molecular switch controlling the induction of the virus from latency. For these studies, we have developed a number of quantitative assays for measuring viral reactivation and replication in response to various proteins and stimuli. We have also determined that Rta's critical role in reactivation is to transcriptionally transactivate viral and cellular promoters in combination with other host and viral proteins. We have identified two of these cellular proteins, and we are characterizing the DNA/protein interactions that are critical for viral reactivation. We are also deciphering Rta's function by investigating its mechanisms of interaction with heterologous viral proteins. Finally, we are committed to determining the molecular regulation of progression of the viral lytic cycle in which many of the viral oncogenes are expressed.