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Up to 10% of the mouse genome is comprised of endogenous retrovirus (ERV) sequences, and most represent the remains of ancient
germ line infections. Our knowledge of the three distinct classes of ERVs is inversely correlated with their copy number,
and their characterization has benefited from the availability of divergent wild mouse species and subspecies, and from ongoing
analysis of the Mus genome sequence. In contrast to human ERVs, which are nearly all extinct, active mouse ERVs can still be found in all three
ERV classes. The distribution and diversity of ERVs has been shaped by host-virus interactions over the course of evolution,
but ERVs have also been pivotal in shaping the mouse genome by altering host genes through insertional mutagenesis, by adding
novel regulatory and coding sequences, and by their co-option by host cells as retroviral resistance genes. We review mechanisms
by which an adaptive coexistence has evolved. (Part of a Multiauthor Review) 相似文献
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Blikstad V Benachenhou F Sperber GO Blomberg J 《Cellular and molecular life sciences : CMLS》2008,65(21):3348-3365
Endogenous retroviruses (ERVs) most likely are remnants of ancient retroviral infections. ERVs preserve functions of exogenous
retroviruses to a varying extent, and can be parasites, symbionts or more or less neutral genetic ‘junk’.Their evolution has
two facets, pre- and post-endogenization. Although the two are not clearly separated, the first pertains to retroviral evolution
in general and the second to the fate of repetitive DNA and the evolution of the host organism and its genome. The study of
ERVs provides much material for the understanding of retroviral evolution. This sequence archive reflects the history of successes
and shortcomings of antiviral resistance, but also of strategic evolutionary decisions regarding genome organization and new
gene acquisition. This review discusses retroviral evolution illustrated through HERVs, bioinformatic prerequisites for ERV
studies, the endogenization process and HERV evolution post-endogenization, including relation to disease. (Part of a Multi-author
Review) 相似文献
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Santoro R 《Cellular and molecular life sciences : CMLS》2005,62(18):2067-2079
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Ruprecht K Mayer J Sauter M Roemer K Mueller-Lantzsch N 《Cellular and molecular life sciences : CMLS》2008,65(21):3366-3382
The genomes of vertebrates contain sequences that are similar to present-day exogenous retroviruses. Such sequences, called
endogenous retroviruses (ERVs), have resulted from ancestral germ line infections by exogenous retroviruses which have thereafter
been transmitted in a Mendelian fashion. By analogy to exogenous tumorigenic retroviruses, ERVs have been implicated in the
pathogenesis of cancer. Cumulative evidence from animal models indicates that ERVs may participate in the process of malignant
transformation or promote tumor growth, e.g. through insertional mutagenesis or via counteracting tumor immunosurveillance.
Here, we review the role of ERVs in tumorigenesis with focus on human ERVs (HERVs) in human cancer. Although available data
suggest a potential role of HERVs in human cancers, in particular germ cell tumors, the contributions of HERVs to human tumorigenesis
warrant further elucidation. (Part of a Multi-author Review) 相似文献
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RNA-mediated gene silencing 总被引:21,自引:0,他引:21
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El-Osta A 《Cellular and molecular life sciences : CMLS》2004,61(17):2135-2136
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Silencing of DNA repair genes plays a critical role in the development of the cancer because these genes, functioning normally, would prevent the accumulation of mutations leading to carcinogenesis. Epigenetic gene silencing is an alternative mechanism to genetic gene aberration, inactivating those genes in cancer. DNA methylation and histone modification are the major factors for epigenetic regulation of gene expression. Here, we describe recent advances in understanding of epigenetic silencing of DNA repair genes and their epigenetic mechanisms involving DNA methylation and histone modification. 相似文献