Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/38142
Title: The cytoskeleton adaptor protein ankyrin-1 is upregulated by p53 following DNA damage and alters cell migration
Authors: Hall, A. E.
Lu, W. T.
Godfrey, J. D.
Antonov, A. V.
Paicu, C.
Moxon, S.
Dalmay, T.
Wilczynska, A.
Muller, P. A.
Bushell, Martin D.
First Published: 7-Apr-2016
Publisher: Nature Publishing Group for Associazione Differenziamento e Morte Cellulare
Citation: Cell Death and Disease , 2016, 7, e2184
Abstract: The integrity of the genome is maintained by a host of surveillance and repair mechanisms that are pivotal for cellular function. The tumour suppressor protein p53 is a major component of the DNA damage response pathway and plays a vital role in the maintenance of cell-cycle checkpoints. Here we show that a microRNA, miR-486, and its host gene ankyrin-1 (ANK1) are induced by p53 following DNA damage. Strikingly, the cytoskeleton adaptor protein ankyrin-1 was induced over 80-fold following DNA damage. ANK1 is upregulated in response to a variety of DNA damage agents in a range of cell types. We demonstrate that miR-486-5p is involved in controlling G1/S transition following DNA damage, whereas the induction of the ankyrin-1 protein alters the structure of the actin cytoskeleton and sustains limited cell migration during DNA damage. Importantly, we found that higher ANK1 expression correlates with decreased survival in cancer patients. Thus, these observations highlight ANK1 as an important effector downstream of the p53 pathway.
DOI Link: 10.1038/cddis.2016.91
eISSN: 2041-4889
Links: http://www.nature.com/cddis/journal/v7/n4/full/cddis201691a.html
http://hdl.handle.net/2381/38142
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © Macmillan Publishers Limited, 2016. This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/ ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Appears in Collections:Published Articles, MRC Toxicology Unit

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