Insulin receptor substrate 4 (IRS4) is a constitutive active oncogenic driver collaborating with HER2 and causing therapeutic resistance

Insulin receptor substrate 4 (IRS4) belongs to a family of cytoplasmic docking proteins mediating signals from cell surface receptors to downstream effectors. While IRS1 and IRS2 mediate signals from an active receptor, we found that IRS4 hyperactivates the phosphatidylinositol phosphate kinase (PI3...

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Detalles Bibliográficos
Autores principales: Ikink, Gerjon J., Hilkens, John
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2017
Materias:
Author's View
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383353/
https://www.ncbi.nlm.nih.gov/pubmed/28401183
http://dx.doi.org/10.1080/23723556.2017.1279722
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author Ikink, Gerjon J.
Hilkens, John
author_facet Ikink, Gerjon J.
Hilkens, John
author_sort Ikink, Gerjon J.
collection PubMed
description Insulin receptor substrate 4 (IRS4) belongs to a family of cytoplasmic docking proteins mediating signals from cell surface receptors to downstream effectors. While IRS1 and IRS2 mediate signals from an active receptor, we found that IRS4 hyperactivates the phosphatidylinositol phosphate kinase (PI3K)-pathway independent of upstream signals and is irresponsive to feedback regulation causing cancer and resistance to human epidermal growth factor receptor 2 (HER2) targeted therapy.
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spelling pubmed-53833532018-01-17 Insulin receptor substrate 4 (IRS4) is a constitutive active oncogenic driver collaborating with HER2 and causing therapeutic resistance Ikink, Gerjon J. Hilkens, John Mol Cell Oncol Author's View Insulin receptor substrate 4 (IRS4) belongs to a family of cytoplasmic docking proteins mediating signals from cell surface receptors to downstream effectors. While IRS1 and IRS2 mediate signals from an active receptor, we found that IRS4 hyperactivates the phosphatidylinositol phosphate kinase (PI3K)-pathway independent of upstream signals and is irresponsive to feedback regulation causing cancer and resistance to human epidermal growth factor receptor 2 (HER2) targeted therapy. Taylor & Francis 2017-01-17 /pmc/articles/PMC5383353/ /pubmed/28401183 http://dx.doi.org/10.1080/23723556.2017.1279722 Text en © 2017 The Author(s). Published with license by Taylor & Francis Group, LLC http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.
spellingShingle Author's View
Ikink, Gerjon J.
Hilkens, John
Insulin receptor substrate 4 (IRS4) is a constitutive active oncogenic driver collaborating with HER2 and causing therapeutic resistance
title Insulin receptor substrate 4 (IRS4) is a constitutive active oncogenic driver collaborating with HER2 and causing therapeutic resistance
title_full Insulin receptor substrate 4 (IRS4) is a constitutive active oncogenic driver collaborating with HER2 and causing therapeutic resistance
title_fullStr Insulin receptor substrate 4 (IRS4) is a constitutive active oncogenic driver collaborating with HER2 and causing therapeutic resistance
title_full_unstemmed Insulin receptor substrate 4 (IRS4) is a constitutive active oncogenic driver collaborating with HER2 and causing therapeutic resistance
title_short Insulin receptor substrate 4 (IRS4) is a constitutive active oncogenic driver collaborating with HER2 and causing therapeutic resistance
title_sort insulin receptor substrate 4 (irs4) is a constitutive active oncogenic driver collaborating with her2 and causing therapeutic resistance
topic Author's View
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383353/
https://www.ncbi.nlm.nih.gov/pubmed/28401183
http://dx.doi.org/10.1080/23723556.2017.1279722
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