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AKT/GSK3β Signaling in Glioblastoma
Glioblastoma (GBM) is the most aggressive of primary brain tumors. Despite the progress in understanding the biology of the pathogenesis of glioma made during the past decade, the clinical outcome of patients with GBM remains still poor. Deregulation of many signaling pathways involved in growth, su...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5357492/ https://www.ncbi.nlm.nih.gov/pubmed/27568206 http://dx.doi.org/10.1007/s11064-016-2044-4 |
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author | Majewska, Ewelina Szeliga, Monika |
author_facet | Majewska, Ewelina Szeliga, Monika |
author_sort | Majewska, Ewelina |
collection | PubMed |
description | Glioblastoma (GBM) is the most aggressive of primary brain tumors. Despite the progress in understanding the biology of the pathogenesis of glioma made during the past decade, the clinical outcome of patients with GBM remains still poor. Deregulation of many signaling pathways involved in growth, survival, migration and resistance to treatment has been implicated in pathogenesis of GBM. One of these pathways is phosphatidylinositol-3 kinases (PI3K)/protein kinase B (AKT)/rapamycin-sensitive mTOR-complex (mTOR) pathway, intensively studied and widely described so far. Much less attention has been paid to the role of glycogen synthase kinase 3 β (GSK3β), a target of AKT. In this review we focus on the function of AKT/GSK3β signaling in GBM. |
format | Online Article Text |
id | pubmed-5357492 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-53574922017-03-30 AKT/GSK3β Signaling in Glioblastoma Majewska, Ewelina Szeliga, Monika Neurochem Res Original Paper Glioblastoma (GBM) is the most aggressive of primary brain tumors. Despite the progress in understanding the biology of the pathogenesis of glioma made during the past decade, the clinical outcome of patients with GBM remains still poor. Deregulation of many signaling pathways involved in growth, survival, migration and resistance to treatment has been implicated in pathogenesis of GBM. One of these pathways is phosphatidylinositol-3 kinases (PI3K)/protein kinase B (AKT)/rapamycin-sensitive mTOR-complex (mTOR) pathway, intensively studied and widely described so far. Much less attention has been paid to the role of glycogen synthase kinase 3 β (GSK3β), a target of AKT. In this review we focus on the function of AKT/GSK3β signaling in GBM. Springer US 2016-08-27 2017 /pmc/articles/PMC5357492/ /pubmed/27568206 http://dx.doi.org/10.1007/s11064-016-2044-4 Text en © The Author(s) 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
spellingShingle | Original Paper Majewska, Ewelina Szeliga, Monika AKT/GSK3β Signaling in Glioblastoma |
title | AKT/GSK3β Signaling in Glioblastoma |
title_full | AKT/GSK3β Signaling in Glioblastoma |
title_fullStr | AKT/GSK3β Signaling in Glioblastoma |
title_full_unstemmed | AKT/GSK3β Signaling in Glioblastoma |
title_short | AKT/GSK3β Signaling in Glioblastoma |
title_sort | akt/gsk3β signaling in glioblastoma |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5357492/ https://www.ncbi.nlm.nih.gov/pubmed/27568206 http://dx.doi.org/10.1007/s11064-016-2044-4 |
work_keys_str_mv | AT majewskaewelina aktgsk3bsignalinginglioblastoma AT szeligamonika aktgsk3bsignalinginglioblastoma |