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Death Associated Protein Kinase 1 (DAPK1): A Regulator of Apoptosis and Autophagy
Death-Associated Protein Kinase 1 (DAPK1) belongs to a family of five serine/threonine (Ser/Thr) kinases that possess tumor suppressive function and also mediate a wide range of cellular processes, including apoptosis and autophagy. The loss and gain-of–function of DAPK1 is associated with various c...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2016
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4917528/ https://www.ncbi.nlm.nih.gov/pubmed/27445685 http://dx.doi.org/10.3389/fnmol.2016.00046 |
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author | Singh, Pratibha Ravanan, Palaniyandi Talwar, Priti |
author_facet | Singh, Pratibha Ravanan, Palaniyandi Talwar, Priti |
author_sort | Singh, Pratibha |
collection | PubMed |
description | Death-Associated Protein Kinase 1 (DAPK1) belongs to a family of five serine/threonine (Ser/Thr) kinases that possess tumor suppressive function and also mediate a wide range of cellular processes, including apoptosis and autophagy. The loss and gain-of–function of DAPK1 is associated with various cancer and neurodegenerative diseases respectively. In recent years, mechanistic studies have broadened our knowledge of the molecular mechanisms involved in DAPK1-mediated autophagy/apoptosis. In the present review, we have discussed the structural information and various cellular functions of DAPK1 in a comprehensive manner. |
format | Online Article Text |
id | pubmed-4917528 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-49175282016-07-21 Death Associated Protein Kinase 1 (DAPK1): A Regulator of Apoptosis and Autophagy Singh, Pratibha Ravanan, Palaniyandi Talwar, Priti Front Mol Neurosci Neuroscience Death-Associated Protein Kinase 1 (DAPK1) belongs to a family of five serine/threonine (Ser/Thr) kinases that possess tumor suppressive function and also mediate a wide range of cellular processes, including apoptosis and autophagy. The loss and gain-of–function of DAPK1 is associated with various cancer and neurodegenerative diseases respectively. In recent years, mechanistic studies have broadened our knowledge of the molecular mechanisms involved in DAPK1-mediated autophagy/apoptosis. In the present review, we have discussed the structural information and various cellular functions of DAPK1 in a comprehensive manner. Frontiers Media S.A. 2016-06-23 /pmc/articles/PMC4917528/ /pubmed/27445685 http://dx.doi.org/10.3389/fnmol.2016.00046 Text en Copyright © 2016 Singh, Ravanan and Talwar. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Singh, Pratibha Ravanan, Palaniyandi Talwar, Priti Death Associated Protein Kinase 1 (DAPK1): A Regulator of Apoptosis and Autophagy |
title | Death Associated Protein Kinase 1 (DAPK1): A Regulator of Apoptosis and Autophagy |
title_full | Death Associated Protein Kinase 1 (DAPK1): A Regulator of Apoptosis and Autophagy |
title_fullStr | Death Associated Protein Kinase 1 (DAPK1): A Regulator of Apoptosis and Autophagy |
title_full_unstemmed | Death Associated Protein Kinase 1 (DAPK1): A Regulator of Apoptosis and Autophagy |
title_short | Death Associated Protein Kinase 1 (DAPK1): A Regulator of Apoptosis and Autophagy |
title_sort | death associated protein kinase 1 (dapk1): a regulator of apoptosis and autophagy |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4917528/ https://www.ncbi.nlm.nih.gov/pubmed/27445685 http://dx.doi.org/10.3389/fnmol.2016.00046 |
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