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To live or let die – complexity within the E2F1 pathway

The E2F1 transcription factor is a recognized regulator of the cell cycle as well as a potent mediator of DNA damage-induced apoptosis and the checkpoint response. Understanding the diverse and seemingly dichotomous functions of E2F1 activity has been the focus of extensive ongoing research. Althoug...

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Detalles Bibliográficos
Autores principales: Poppy Roworth, A, Ghari, Fatemeh, La Thangue, Nicholas B
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4905241/
https://www.ncbi.nlm.nih.gov/pubmed/27308406
http://dx.doi.org/10.4161/23723548.2014.970480
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author Poppy Roworth, A
Ghari, Fatemeh
La Thangue, Nicholas B
author_facet Poppy Roworth, A
Ghari, Fatemeh
La Thangue, Nicholas B
author_sort Poppy Roworth, A
collection PubMed
description The E2F1 transcription factor is a recognized regulator of the cell cycle as well as a potent mediator of DNA damage-induced apoptosis and the checkpoint response. Understanding the diverse and seemingly dichotomous functions of E2F1 activity has been the focus of extensive ongoing research. Although the E2F pathway is frequently deregulated in cancer, the contributions of E2F1 itself to tumorigenesis, as a promoter of proliferation or cell death, are far from understood. In this review we aim to provide an update on our current understanding of E2F1, with particular insight into its novel interaction partners and post-translational modifications, as a means to explaining its diverse functional complexity.
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spelling pubmed-49052412016-06-15 To live or let die – complexity within the E2F1 pathway Poppy Roworth, A Ghari, Fatemeh La Thangue, Nicholas B Mol Cell Oncol Review The E2F1 transcription factor is a recognized regulator of the cell cycle as well as a potent mediator of DNA damage-induced apoptosis and the checkpoint response. Understanding the diverse and seemingly dichotomous functions of E2F1 activity has been the focus of extensive ongoing research. Although the E2F pathway is frequently deregulated in cancer, the contributions of E2F1 itself to tumorigenesis, as a promoter of proliferation or cell death, are far from understood. In this review we aim to provide an update on our current understanding of E2F1, with particular insight into its novel interaction partners and post-translational modifications, as a means to explaining its diverse functional complexity. Taylor & Francis 2015-01-30 /pmc/articles/PMC4905241/ /pubmed/27308406 http://dx.doi.org/10.4161/23723548.2014.970480 Text en © 2015 The Author(s). Published with license by Taylor & Francis Group, LLC http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License http://creativecommons.org/licenses/by-nc/3.0/, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
spellingShingle Review
Poppy Roworth, A
Ghari, Fatemeh
La Thangue, Nicholas B
To live or let die – complexity within the E2F1 pathway
title To live or let die – complexity within the E2F1 pathway
title_full To live or let die – complexity within the E2F1 pathway
title_fullStr To live or let die – complexity within the E2F1 pathway
title_full_unstemmed To live or let die – complexity within the E2F1 pathway
title_short To live or let die – complexity within the E2F1 pathway
title_sort to live or let die – complexity within the e2f1 pathway
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4905241/
https://www.ncbi.nlm.nih.gov/pubmed/27308406
http://dx.doi.org/10.4161/23723548.2014.970480
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