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Background: Increased transcription of the human endogenous retrovirus group HERV-K (HML-2) is often seen during disease. Although the mechanism of its tissue-specific activation is unclear, research shows that LTR CpG hypomethylation alone is not sufficient to induce its promoter activity and that the transcriptional milieu of a malignant cell contributes, at least partly, to differential HML-2 ... read moreexpression.
Keywords: Endogenous retrovirus, HERV-K, HML-2, LTR, Transcription, Tumorigenesis.
Springer Open.read less
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