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Targeting Promyelocytic Leukemia Protein: A Means to Regulating PML Nuclear Bodies

The promyelocytic leukemia protein (PML) is involved in many cellular processes including cell cycle progression, DNA damage response, transcriptional regulation, viral infection, and apoptosis. These cellular activities often rely on the localization of PML to unique subnuclear structures known as...

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Detalles Bibliográficos
Autores principales: Reineke, Erin L., Kao, Hung-Ying
Formato: Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2686094/
https://www.ncbi.nlm.nih.gov/pubmed/19471587
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author Reineke, Erin L.
Kao, Hung-Ying
author_facet Reineke, Erin L.
Kao, Hung-Ying
author_sort Reineke, Erin L.
collection PubMed
description The promyelocytic leukemia protein (PML) is involved in many cellular processes including cell cycle progression, DNA damage response, transcriptional regulation, viral infection, and apoptosis. These cellular activities often rely on the localization of PML to unique subnuclear structures known as PML nuclear bodies (NBs). More than 50 cellular proteins are known to traffic in and out of PML NBs, either transiently or constitutively. In order to understand the dynamics of these NBs, it is important to delineate the regulation of PML itself. PML is subject to extensive regulation at transcriptional, post-transcriptional, and post-translational levels. Many of these modes of regulation depend on the cellular context and the presence of extracellular signals. This review focuses on the current knowledge of regulation of PML under normal cellular conditions as well as the role for regulation of PML in viral infection and cancer.
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spelling pubmed-26860942009-05-26 Targeting Promyelocytic Leukemia Protein: A Means to Regulating PML Nuclear Bodies Reineke, Erin L. Kao, Hung-Ying Int J Biol Sci Review The promyelocytic leukemia protein (PML) is involved in many cellular processes including cell cycle progression, DNA damage response, transcriptional regulation, viral infection, and apoptosis. These cellular activities often rely on the localization of PML to unique subnuclear structures known as PML nuclear bodies (NBs). More than 50 cellular proteins are known to traffic in and out of PML NBs, either transiently or constitutively. In order to understand the dynamics of these NBs, it is important to delineate the regulation of PML itself. PML is subject to extensive regulation at transcriptional, post-transcriptional, and post-translational levels. Many of these modes of regulation depend on the cellular context and the presence of extracellular signals. This review focuses on the current knowledge of regulation of PML under normal cellular conditions as well as the role for regulation of PML in viral infection and cancer. Ivyspring International Publisher 2009-05-22 /pmc/articles/PMC2686094/ /pubmed/19471587 Text en © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.
spellingShingle Review
Reineke, Erin L.
Kao, Hung-Ying
Targeting Promyelocytic Leukemia Protein: A Means to Regulating PML Nuclear Bodies
title Targeting Promyelocytic Leukemia Protein: A Means to Regulating PML Nuclear Bodies
title_full Targeting Promyelocytic Leukemia Protein: A Means to Regulating PML Nuclear Bodies
title_fullStr Targeting Promyelocytic Leukemia Protein: A Means to Regulating PML Nuclear Bodies
title_full_unstemmed Targeting Promyelocytic Leukemia Protein: A Means to Regulating PML Nuclear Bodies
title_short Targeting Promyelocytic Leukemia Protein: A Means to Regulating PML Nuclear Bodies
title_sort targeting promyelocytic leukemia protein: a means to regulating pml nuclear bodies
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2686094/
https://www.ncbi.nlm.nih.gov/pubmed/19471587
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