Review
Version 1
Preserved in Portico This version is not peer-reviewed
The Role of JMY in p53 Regulation.
Version 1
: Received: 13 April 2018 / Approved: 13 April 2018 / Online: 13 April 2018 (14:55:47 CEST)
Version 2 : Received: 17 April 2018 / Approved: 18 April 2018 / Online: 18 April 2018 (13:46:19 CEST)
Version 2 : Received: 17 April 2018 / Approved: 18 April 2018 / Online: 18 April 2018 (13:46:19 CEST)
A peer-reviewed article of this Preprint also exists.
Adighibe, O.; Pezzella, F. The Role of JMY in p53 Regulation. Cancers 2018, 10, 173. Adighibe, O.; Pezzella, F. The Role of JMY in p53 Regulation. Cancers 2018, 10, 173.
Abstract
Following an event damaging the DNA, p53 levels increases inducing cell cycle arrest or apoptosis. JMY protein is a transcription co-factor involved in p53 regulation. After a DNA damage, also JMY levels increase and, as this protein accumulates in the nucleus, it forms a complex with P300 and Strap1 which increases the ability of p53 to induce transcription of proteins triggering apoptosis but not cell cycle. Therefore, Increase levels of JMY “direct” p53 activity toward triggering apoptosis. JMY expression is also linked to increased motility as it downregulates the expression of adhesion molecules of the Cadherin family and induces actin nucleation, making the cell less adhesive and more mobile. According to the scenario this gene can therefore have both a suppressive or a tumour promoting activity.
Keywords
p53, JMY, regulation, apoptosis, motility
Subject
Medicine and Pharmacology, Oncology and Oncogenics
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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