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Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking

Vesicular trafficking events play key roles in the compartmentalization and proper sorting of cellular components. These events have crucial roles in sensing external signals, regulating protein activities and stimulating cell growth or death decisions. Although mutations in vesicle trafficking play...

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Detalles Bibliográficos
Autores principales: Fraser, Jane, Cabodevilla, Ainara G., Simpson, Joanne, Gammoh, Noor
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5869858/
https://www.ncbi.nlm.nih.gov/pubmed/29233871
http://dx.doi.org/10.1042/EBC20170091
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author Fraser, Jane
Cabodevilla, Ainara G.
Simpson, Joanne
Gammoh, Noor
author_facet Fraser, Jane
Cabodevilla, Ainara G.
Simpson, Joanne
Gammoh, Noor
author_sort Fraser, Jane
collection PubMed
description Vesicular trafficking events play key roles in the compartmentalization and proper sorting of cellular components. These events have crucial roles in sensing external signals, regulating protein activities and stimulating cell growth or death decisions. Although mutations in vesicle trafficking players are not direct drivers of cellular transformation, their activities are important in facilitating oncogenic pathways. One such pathway is the sensing of external stimuli and signalling through receptor tyrosine kinases (RTKs). The regulation of RTK activity by the endocytic pathway has been extensively studied. Compelling recent studies have begun to highlight the association between autophagy and RTK signalling. The influence of this interplay on cellular status and its relevance in disease settings will be discussed here.
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spelling pubmed-58698582018-04-05 Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking Fraser, Jane Cabodevilla, Ainara G. Simpson, Joanne Gammoh, Noor Essays Biochem Review Articles Vesicular trafficking events play key roles in the compartmentalization and proper sorting of cellular components. These events have crucial roles in sensing external signals, regulating protein activities and stimulating cell growth or death decisions. Although mutations in vesicle trafficking players are not direct drivers of cellular transformation, their activities are important in facilitating oncogenic pathways. One such pathway is the sensing of external stimuli and signalling through receptor tyrosine kinases (RTKs). The regulation of RTK activity by the endocytic pathway has been extensively studied. Compelling recent studies have begun to highlight the association between autophagy and RTK signalling. The influence of this interplay on cellular status and its relevance in disease settings will be discussed here. Portland Press Ltd. 2017-12-12 /pmc/articles/PMC5869858/ /pubmed/29233871 http://dx.doi.org/10.1042/EBC20170091 Text en © 2017 The Author(s). https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY-NC-ND) (https://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Review Articles
Fraser, Jane
Cabodevilla, Ainara G.
Simpson, Joanne
Gammoh, Noor
Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking
title Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking
title_full Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking
title_fullStr Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking
title_full_unstemmed Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking
title_short Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking
title_sort interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5869858/
https://www.ncbi.nlm.nih.gov/pubmed/29233871
http://dx.doi.org/10.1042/EBC20170091
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