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p53 in the game of transposons
Abstract
Throughout the animal kingdom, p53 genes function to restrain mobile elements and recent observations indicate that transposons become derepressed in human cancers. Together, these emerging lines of evidence suggest that cancers driven by p53 mutations could represent “transpospoathies,” i.e. disease states linked to eruptions of mobile elements. The transposopathy hypothesis predicts that p53 acts through conserved mechanisms to contain transposon movement, and in this way, prevents tumor formation. How transposon eruptions provoke neoplasias is not well understood but, from a broader perspective, this hypothesis also provides an attractive framework to explore unrestrained mobile elements as inciters of late‐onset idiopathic disease. Also see the video abstract here.
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“Importantly, TEs and ERVs are both associated with (and could be the primary cause of) several diseases [15 -17].”
From The case for not masking away repetitive DNA (2018) · cites this paper as [16]
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Cited by
Sorted by citations
The case for not masking away repetitive DNA
Slotkin, R. K. (2018) · Mobile DNA · doi:10.1186/s13100-018-0120-9 · Cited by 61
Metadata
- Authors
- Wylie, A., Jones, A. E., & Abrams, J. M.
- Venue
- BioEssays
- Publisher
- Wiley
- Published
- 2016-09-19
- Volume
- 38
- Issue
- 11
- Pages
- 1111-1116
- ISSN
- 0265-9247
- 1521-1878
- PMC
- PMC5142446
- Cited by
- 29
- References
- 10
- Language
- en
- Funders
- American Cancer Society (128847‐PF‐15‐160‐01‐DDC)
- Welch Foundation (I‐1865)
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