Title | NF-κB as a target for oncogenic viruses. |
Publication Type | Journal Article |
Year of Publication | 2011 |
Authors | Sun S-C, Cesarman E |
Journal | Curr Top Microbiol Immunol |
Volume | 349 |
Pagination | 197-244 |
Date Published | 2011 |
ISSN | 0070-217X |
Keywords | Animals, Herpesvirus 4, Human, Herpesvirus 8, Human, Human T-lymphotropic virus 1, Humans, NF-kappa B, Oncogene Proteins, Viral, Signal Transduction |
Abstract | NF-κB is a pivotal transcription factor that controls cell survival and proliferation in diverse physiological processes. The activity of NF-κB is tightly controlled through its cytoplasmic sequestration by specific inhibitors, IκBs. Various cellular stimuli induce the activation of an IκB kinase, which phosphorylates IκBs and triggers their proteasomal degradation, causing nuclear translocation of activated NF-κB. Under normal conditions, the activation of NF-κB occurs transiently, thus ensuring rapid but temporary induction of target genes. Deregulated NF-κB activation contributes to the development of various diseases, including cancers and immunological disorders. Accumulated studies demonstrate that the NF-κB signaling pathway is a target of several human oncogenic viruses, including the human T cell leukemia virus type 1, the Kaposi sarcoma-associated herpesvirus, and the Epstein-Bar virus. These viruses encode specific oncoproteins that target different signaling components of the NF-κB pathway, leading to persistent activation of NF-κB. This chapter will discuss the molecular mechanisms by which NF-κB is activated by the viral oncoproteins. |
DOI | 10.1007/82_2010_108 |
Alternate Journal | Curr Top Microbiol Immunol |
PubMed ID | 20845110 |
Grant List | GM084459 / GM / NIGMS NIH HHS / United States AI057555 / AI / NIAID NIH HHS / United States AI064639 / AI / NIAID NIH HHS / United States CA103646 / CA / NCI NIH HHS / United States CA068939 / CA / NCI NIH HHS / United States |
Related Faculty:
Ethel Cesarman, M.D., Ph.D.