A model for genetic and epigenetic regulatory networks identifies rare pathways for transcription factor induced pluripotency.

With relatively low efficiency, differentiated cells can be reprogrammed to a pluripotent state by ectopic expression of a few transcription factors. An understanding of the mechanisms that underlie data emerging from such experiments can help design optimal strategies for creating pluripotent cells...

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Main Authors: Maxim N Artyomov, Alexander Meissner, Arup K Chakraborty
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2010-05-01
Series:PLoS Computational Biology
Online Access:http://europepmc.org/articles/PMC2869311?pdf=render
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spelling doaj-1684f565167e4f849973b93c4f5884652020-11-24T21:55:55ZengPublic Library of Science (PLoS)PLoS Computational Biology1553-734X1553-73582010-05-0165e100078510.1371/journal.pcbi.1000785A model for genetic and epigenetic regulatory networks identifies rare pathways for transcription factor induced pluripotency.Maxim N ArtyomovAlexander MeissnerArup K ChakrabortyWith relatively low efficiency, differentiated cells can be reprogrammed to a pluripotent state by ectopic expression of a few transcription factors. An understanding of the mechanisms that underlie data emerging from such experiments can help design optimal strategies for creating pluripotent cells for patient-specific regenerative medicine. We have developed a computational model for the architecture of the epigenetic and genetic regulatory networks which describes transformations resulting from expression of reprogramming factors. Importantly, our studies identify the rare temporal pathways that result in induced pluripotent cells. Further experimental tests of predictions emerging from our model should lead to fundamental advances in our understanding of how cellular identity is maintained and transformed.http://europepmc.org/articles/PMC2869311?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Maxim N Artyomov
Alexander Meissner
Arup K Chakraborty
spellingShingle Maxim N Artyomov
Alexander Meissner
Arup K Chakraborty
A model for genetic and epigenetic regulatory networks identifies rare pathways for transcription factor induced pluripotency.
PLoS Computational Biology
author_facet Maxim N Artyomov
Alexander Meissner
Arup K Chakraborty
author_sort Maxim N Artyomov
title A model for genetic and epigenetic regulatory networks identifies rare pathways for transcription factor induced pluripotency.
title_short A model for genetic and epigenetic regulatory networks identifies rare pathways for transcription factor induced pluripotency.
title_full A model for genetic and epigenetic regulatory networks identifies rare pathways for transcription factor induced pluripotency.
title_fullStr A model for genetic and epigenetic regulatory networks identifies rare pathways for transcription factor induced pluripotency.
title_full_unstemmed A model for genetic and epigenetic regulatory networks identifies rare pathways for transcription factor induced pluripotency.
title_sort model for genetic and epigenetic regulatory networks identifies rare pathways for transcription factor induced pluripotency.
publisher Public Library of Science (PLoS)
series PLoS Computational Biology
issn 1553-734X
1553-7358
publishDate 2010-05-01
description With relatively low efficiency, differentiated cells can be reprogrammed to a pluripotent state by ectopic expression of a few transcription factors. An understanding of the mechanisms that underlie data emerging from such experiments can help design optimal strategies for creating pluripotent cells for patient-specific regenerative medicine. We have developed a computational model for the architecture of the epigenetic and genetic regulatory networks which describes transformations resulting from expression of reprogramming factors. Importantly, our studies identify the rare temporal pathways that result in induced pluripotent cells. Further experimental tests of predictions emerging from our model should lead to fundamental advances in our understanding of how cellular identity is maintained and transformed.
url http://europepmc.org/articles/PMC2869311?pdf=render
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