| pubmed-article:20724161 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20724161 | lifeskim:mentions | umls-concept:C0521026 | lld:lifeskim |
| pubmed-article:20724161 | lifeskim:mentions | umls-concept:C0599840 | lld:lifeskim |
| pubmed-article:20724161 | lifeskim:mentions | umls-concept:C1167395 | lld:lifeskim |
| pubmed-article:20724161 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:20724161 | lifeskim:mentions | umls-concept:C1655731 | lld:lifeskim |
| pubmed-article:20724161 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
| pubmed-article:20724161 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:20724161 | pubmed:dateCreated | 2010-9-27 | lld:pubmed |
| pubmed-article:20724161 | pubmed:abstractText | One of the key questions in the study of mammalian gene regulation is how epigenetic methylation patterns on histones and DNA are initiated and established. These stable, heritable, covalent modifications are largely associated with the repression or silencing of gene transcription, and when deregulated can be involved in the development of human diseases such as cancer. This article reviews examples of viruses and bacteria known or thought to induce epigenetic changes in host cells, and how this might contribute to disease. The heritable nature of these processes in gene regulation suggests that they could play important roles in chronic diseases associated with microbial persistence; they might also explain so-called 'hit-and-run' phenomena in infectious disease pathogenesis. | lld:pubmed |
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