YAP enters the mTOR pathway to promote tuberous sclerosis complex

Mutations in tuberous sclerosis complex 1 (TSC1) or TSC2 predispose to angiomyolipomas and lymphangioleiomyomatosis in a mTOR-dependent manner. In these mesenchymal lesions, mTOR suppresses macroautophagy-mediated lysosomal degradation of YAP, which is a transcriptional coactivator of Hippo pathway...

Descripción completa

Detalles Bibliográficos
Autores principales: Liang, Ning, Pende, Mario
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2015
Materias:
Commentary
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4905364/
https://www.ncbi.nlm.nih.gov/pubmed/27308518
http://dx.doi.org/10.1080/23723556.2014.998100
_version_ 1782437253627248640
author Liang, Ning
Pende, Mario
author_facet Liang, Ning
Pende, Mario
author_sort Liang, Ning
collection PubMed
description Mutations in tuberous sclerosis complex 1 (TSC1) or TSC2 predispose to angiomyolipomas and lymphangioleiomyomatosis in a mTOR-dependent manner. In these mesenchymal lesions, mTOR suppresses macroautophagy-mediated lysosomal degradation of YAP, which is a transcriptional coactivator of Hippo pathway and is required for the tumorigenesis of TSC. Therapeutic applications for TSC and other diseases with dysregulated mTOR activity can be envisaged.
format Online
Article
Text
id pubmed-4905364
institution National Center for Biotechnology Information
language English
publishDate 2015
publisher Taylor & Francis
record_format MEDLINE/PubMed
spelling pubmed-49053642016-06-15 YAP enters the mTOR pathway to promote tuberous sclerosis complex Liang, Ning Pende, Mario Mol Cell Oncol Commentary Mutations in tuberous sclerosis complex 1 (TSC1) or TSC2 predispose to angiomyolipomas and lymphangioleiomyomatosis in a mTOR-dependent manner. In these mesenchymal lesions, mTOR suppresses macroautophagy-mediated lysosomal degradation of YAP, which is a transcriptional coactivator of Hippo pathway and is required for the tumorigenesis of TSC. Therapeutic applications for TSC and other diseases with dysregulated mTOR activity can be envisaged. Taylor & Francis 2015-05-01 /pmc/articles/PMC4905364/ /pubmed/27308518 http://dx.doi.org/10.1080/23723556.2014.998100 Text en © 2015 The Author(s). Published with license by Taylor & Francis Group, LLC http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
spellingShingle Commentary
Liang, Ning
Pende, Mario
YAP enters the mTOR pathway to promote tuberous sclerosis complex
title YAP enters the mTOR pathway to promote tuberous sclerosis complex
title_full YAP enters the mTOR pathway to promote tuberous sclerosis complex
title_fullStr YAP enters the mTOR pathway to promote tuberous sclerosis complex
title_full_unstemmed YAP enters the mTOR pathway to promote tuberous sclerosis complex
title_short YAP enters the mTOR pathway to promote tuberous sclerosis complex
title_sort yap enters the mtor pathway to promote tuberous sclerosis complex
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4905364/
https://www.ncbi.nlm.nih.gov/pubmed/27308518
http://dx.doi.org/10.1080/23723556.2014.998100
work_keys_str_mv AT liangning yapentersthemtorpathwaytopromotetuberoussclerosiscomplex
AT pendemario yapentersthemtorpathwaytopromotetuberoussclerosiscomplex

Ejemplares similares