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- W2134263911 abstract "Human tumor viruses are responsible for one-fifth of all cancers worldwide. These viruses have evolved multiple strategies to evade immune defenses and to persist in the host by establishing a latent infection. Proliferation is necessary for pretumor cells to accumulate genetic alterations and to acquire a transformed phenotype. However, each cell division is associated with a progressive shortening of the telomeres, which can suppress tumor development by initiating senescence and irreversible cell cycle arrest. Therefore, the ability of virus-infected cells to circumvent the senescence program is essential for the long-term survival and proliferation of infected cells and the likelihood of transformation. We review the multiple strategies used by human DNA and RNA tumor viruses to subvert telomerase functions during cellular transformation and carcinogenesis. Epstein-Barr virus, Kaposi sarcoma-associated herpesvirus, human papillomavirus, hepatitis B virus, hepatitis C virus, and human T-cell leukemia virus-1 each can increase transcription of the telomerase reverse transcriptase. Several viruses appear to mediate cis-activation or enhance epigenetic activation of telomerase transcription. Epstein-Barr virus and human papillomavirus have each developed posttranscriptional mechanisms to regulate the telomerase protein. Finally, some tumor virus proteins can also negatively regulate telomerase transcription or activity. It is likely that, as future studies further expose the strategies used by viruses to deregulate telomerase activity and control of telomere length, novel mechanisms will emerge and underscore the importance of increased telomerase activity in sustaining virus-infected cells and its potential in therapeutic targeting." @default.
- W2134263911 created "2016-06-24" @default.
- W2134263911 creator A5019279015 @default.
- W2134263911 creator A5025054085 @default.
- W2134263911 date "2008-01-08" @default.
- W2134263911 modified "2023-10-17" @default.
- W2134263911 title "Regulation of Telomerase and Telomeres: Human Tumor Viruses Take Control" @default.
- W2134263911 cites W1523189699 @default.
- W2134263911 cites W1539426772 @default.
- W2134263911 cites W1545398558 @default.
- W2134263911 cites W1547608553 @default.
- W2134263911 cites W1562677361 @default.
- W2134263911 cites W1574658543 @default.
- W2134263911 cites W1578954095 @default.
- W2134263911 cites W1589551152 @default.
- W2134263911 cites W1596304334 @default.
- W2134263911 cites W1685493687 @default.
- W2134263911 cites W1876930771 @default.
- W2134263911 cites W1909882240 @default.
- W2134263911 cites W1956123188 @default.
- W2134263911 cites W1969059360 @default.
- W2134263911 cites W1975562645 @default.
- W2134263911 cites W1977301309 @default.
- W2134263911 cites W1981168810 @default.
- W2134263911 cites W1988379270 @default.
- W2134263911 cites W1990046380 @default.
- W2134263911 cites W1996803249 @default.
- W2134263911 cites W1997988077 @default.
- W2134263911 cites W2002158439 @default.
- W2134263911 cites W2003268750 @default.
- W2134263911 cites W2003862674 @default.
- W2134263911 cites W2010400502 @default.
- W2134263911 cites W2010852984 @default.
- W2134263911 cites W2013059054 @default.
- W2134263911 cites W2013073993 @default.
- W2134263911 cites W2015047103 @default.
- W2134263911 cites W2015352009 @default.
- W2134263911 cites W2016292129 @default.
- W2134263911 cites W2016569877 @default.
- W2134263911 cites W2018513924 @default.
- W2134263911 cites W2020329784 @default.
- W2134263911 cites W2025466551 @default.
- W2134263911 cites W2025728444 @default.
- W2134263911 cites W2027001966 @default.
- W2134263911 cites W2029735450 @default.
- W2134263911 cites W2030642077 @default.
- W2134263911 cites W2036360678 @default.
- W2134263911 cites W2036802367 @default.
- W2134263911 cites W2038982713 @default.
- W2134263911 cites W2039709545 @default.
- W2134263911 cites W2040606106 @default.
- W2134263911 cites W2042707885 @default.
- W2134263911 cites W2044627970 @default.
- W2134263911 cites W2045725116 @default.
- W2134263911 cites W2046002864 @default.
- W2134263911 cites W2047058238 @default.
- W2134263911 cites W2048405417 @default.
- W2134263911 cites W2048962618 @default.
- W2134263911 cites W2054178267 @default.
- W2134263911 cites W2054271458 @default.
- W2134263911 cites W2055086957 @default.
- W2134263911 cites W2055689209 @default.
- W2134263911 cites W2055902044 @default.
- W2134263911 cites W2058349670 @default.
- W2134263911 cites W2061541027 @default.
- W2134263911 cites W2065187149 @default.
- W2134263911 cites W2066410692 @default.
- W2134263911 cites W2070419033 @default.
- W2134263911 cites W2073635566 @default.
- W2134263911 cites W2076361283 @default.
- W2134263911 cites W2076383117 @default.
- W2134263911 cites W2079378073 @default.
- W2134263911 cites W2082999703 @default.
- W2134263911 cites W2084960769 @default.
- W2134263911 cites W2086340898 @default.
- W2134263911 cites W2089380061 @default.
- W2134263911 cites W2092174482 @default.
- W2134263911 cites W2095024877 @default.
- W2134263911 cites W2095519669 @default.
- W2134263911 cites W2098432187 @default.
- W2134263911 cites W2098765233 @default.
- W2134263911 cites W2102268829 @default.
- W2134263911 cites W2102839588 @default.
- W2134263911 cites W2110419228 @default.
- W2134263911 cites W2110796359 @default.
- W2134263911 cites W2114840351 @default.
- W2134263911 cites W2115165466 @default.
- W2134263911 cites W2115346781 @default.
- W2134263911 cites W2115610036 @default.
- W2134263911 cites W2117300924 @default.
- W2134263911 cites W2117605168 @default.
- W2134263911 cites W2118228848 @default.
- W2134263911 cites W2123105653 @default.
- W2134263911 cites W2123422243 @default.
- W2134263911 cites W2127352755 @default.
- W2134263911 cites W2127539269 @default.
- W2134263911 cites W2129306198 @default.
- W2134263911 cites W2130038815 @default.