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Keeping a lid on nodal: transcriptional and translational repression of nodal signalling
Nodal is an evolutionarily conserved member of the transforming growth factor-β (TGF-β) superfamily of secreted signalling factors. Nodal factors are known to play key roles in embryonic development and asymmetry in a variety of organisms ranging from hydra and sea urchins to fish, mice and humans....
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Royal Society
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4736825/ https://www.ncbi.nlm.nih.gov/pubmed/26791244 http://dx.doi.org/10.1098/rsob.150200 |
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author | Sampath, Karuna Robertson, Elizabeth J. |
author_facet | Sampath, Karuna Robertson, Elizabeth J. |
author_sort | Sampath, Karuna |
collection | PubMed |
description | Nodal is an evolutionarily conserved member of the transforming growth factor-β (TGF-β) superfamily of secreted signalling factors. Nodal factors are known to play key roles in embryonic development and asymmetry in a variety of organisms ranging from hydra and sea urchins to fish, mice and humans. In addition to embryonic patterning, Nodal signalling is required for maintenance of human embryonic stem cell pluripotency and mis-regulated Nodal signalling has been found associated with tumour metastases. Therefore, precise and timely regulation of this pathway is essential. Here, we discuss recent evidence from sea urchins, frogs, fish, mice and humans that show a role for transcriptional and translational repression of Nodal signalling during early development. |
format | Online Article Text |
id | pubmed-4736825 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | The Royal Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-47368252016-02-23 Keeping a lid on nodal: transcriptional and translational repression of nodal signalling Sampath, Karuna Robertson, Elizabeth J. Open Biol Review Nodal is an evolutionarily conserved member of the transforming growth factor-β (TGF-β) superfamily of secreted signalling factors. Nodal factors are known to play key roles in embryonic development and asymmetry in a variety of organisms ranging from hydra and sea urchins to fish, mice and humans. In addition to embryonic patterning, Nodal signalling is required for maintenance of human embryonic stem cell pluripotency and mis-regulated Nodal signalling has been found associated with tumour metastases. Therefore, precise and timely regulation of this pathway is essential. Here, we discuss recent evidence from sea urchins, frogs, fish, mice and humans that show a role for transcriptional and translational repression of Nodal signalling during early development. The Royal Society 2016-01-20 /pmc/articles/PMC4736825/ /pubmed/26791244 http://dx.doi.org/10.1098/rsob.150200 Text en © 2016 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 Sampath, Karuna Robertson, Elizabeth J. Keeping a lid on nodal: transcriptional and translational repression of nodal signalling |
title | Keeping a lid on nodal: transcriptional and translational repression of nodal signalling |
title_full | Keeping a lid on nodal: transcriptional and translational repression of nodal signalling |
title_fullStr | Keeping a lid on nodal: transcriptional and translational repression of nodal signalling |
title_full_unstemmed | Keeping a lid on nodal: transcriptional and translational repression of nodal signalling |
title_short | Keeping a lid on nodal: transcriptional and translational repression of nodal signalling |
title_sort | keeping a lid on nodal: transcriptional and translational repression of nodal signalling |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4736825/ https://www.ncbi.nlm.nih.gov/pubmed/26791244 http://dx.doi.org/10.1098/rsob.150200 |
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