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Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different

The ability to regenerate is a fundamental requirement for tissue homeostasis. Regeneration draws on three sources of cells. First and best-studied are dedicated stem/progenitor cells. Second, existing cells may proliferate to compensate for the lost cells of the same type. Third, a different cell t...

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Detalles Bibliográficos
Autor principal: Su, Tin Tin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Royal Society 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6282069/
https://www.ncbi.nlm.nih.gov/pubmed/30487302
http://dx.doi.org/10.1098/rsob.180157
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author Su, Tin Tin
author_facet Su, Tin Tin
author_sort Su, Tin Tin
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description The ability to regenerate is a fundamental requirement for tissue homeostasis. Regeneration draws on three sources of cells. First and best-studied are dedicated stem/progenitor cells. Second, existing cells may proliferate to compensate for the lost cells of the same type. Third, a different cell type may change fate to compensate for the lost cells. This review focuses on regeneration of the third type and will discuss the contributions by post-transcriptional mechanisms including the emerging evidence for cell-autonomous and non-lethal roles of cell death pathways.
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spelling pubmed-62820692018-12-11 Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different Su, Tin Tin Open Biol Review The ability to regenerate is a fundamental requirement for tissue homeostasis. Regeneration draws on three sources of cells. First and best-studied are dedicated stem/progenitor cells. Second, existing cells may proliferate to compensate for the lost cells of the same type. Third, a different cell type may change fate to compensate for the lost cells. This review focuses on regeneration of the third type and will discuss the contributions by post-transcriptional mechanisms including the emerging evidence for cell-autonomous and non-lethal roles of cell death pathways. The Royal Society 2018-11-28 /pmc/articles/PMC6282069/ /pubmed/30487302 http://dx.doi.org/10.1098/rsob.180157 Text en © 2018 The Authors. http://creativecommons.org/licenses/by/4.0/ Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.
spellingShingle Review
Su, Tin Tin
Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different
title Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different
title_full Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different
title_fullStr Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different
title_full_unstemmed Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different
title_short Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different
title_sort cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6282069/
https://www.ncbi.nlm.nih.gov/pubmed/30487302
http://dx.doi.org/10.1098/rsob.180157
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