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Akt inhibitors: mechanism of action and implications for anticancer therapeutics
Akt, better known as protein kinase B (PKB), is a serine/threonine-specific protein kinase which acts as mediator via PI3K/Akt pathway in many biological processes like glucose metabolism, apoptosis, cell differentiation and transcription. Akt1 gene amplification has been implicated in gastric carci...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028840/ https://www.ncbi.nlm.nih.gov/pubmed/24330834 http://dx.doi.org/10.1186/1750-9378-8-49 |
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author | Bhutani, Jaikrit Sheikh, Asfandyar Niazi, Asfandyar Khan |
author_facet | Bhutani, Jaikrit Sheikh, Asfandyar Niazi, Asfandyar Khan |
author_sort | Bhutani, Jaikrit |
collection | PubMed |
description | Akt, better known as protein kinase B (PKB), is a serine/threonine-specific protein kinase which acts as mediator via PI3K/Akt pathway in many biological processes like glucose metabolism, apoptosis, cell differentiation and transcription. Akt1 gene amplification has been implicated in gastric carcinoma while Akt2 amplification has been linked with ovarian, pancreas, breast and stomach tumors. The use of Akt inhibitors as monotherapy or in combination with other anticancer drugs could be useful for combating drug resistance and improving response. Thus, comprehensive understanding of Akt and its linked signaling pathways (PI3K, PKB, mTOR etc.) is necessary to lead to newer drug development and use. |
format | Online Article Text |
id | pubmed-4028840 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-40288402014-05-22 Akt inhibitors: mechanism of action and implications for anticancer therapeutics Bhutani, Jaikrit Sheikh, Asfandyar Niazi, Asfandyar Khan Infect Agent Cancer Letter to the Editor Akt, better known as protein kinase B (PKB), is a serine/threonine-specific protein kinase which acts as mediator via PI3K/Akt pathway in many biological processes like glucose metabolism, apoptosis, cell differentiation and transcription. Akt1 gene amplification has been implicated in gastric carcinoma while Akt2 amplification has been linked with ovarian, pancreas, breast and stomach tumors. The use of Akt inhibitors as monotherapy or in combination with other anticancer drugs could be useful for combating drug resistance and improving response. Thus, comprehensive understanding of Akt and its linked signaling pathways (PI3K, PKB, mTOR etc.) is necessary to lead to newer drug development and use. BioMed Central 2013-12-13 /pmc/articles/PMC4028840/ /pubmed/24330834 http://dx.doi.org/10.1186/1750-9378-8-49 Text en Copyright © 2013 Bhutani et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Letter to the Editor Bhutani, Jaikrit Sheikh, Asfandyar Niazi, Asfandyar Khan Akt inhibitors: mechanism of action and implications for anticancer therapeutics |
title | Akt inhibitors: mechanism of action and implications for anticancer therapeutics |
title_full | Akt inhibitors: mechanism of action and implications for anticancer therapeutics |
title_fullStr | Akt inhibitors: mechanism of action and implications for anticancer therapeutics |
title_full_unstemmed | Akt inhibitors: mechanism of action and implications for anticancer therapeutics |
title_short | Akt inhibitors: mechanism of action and implications for anticancer therapeutics |
title_sort | akt inhibitors: mechanism of action and implications for anticancer therapeutics |
topic | Letter to the Editor |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028840/ https://www.ncbi.nlm.nih.gov/pubmed/24330834 http://dx.doi.org/10.1186/1750-9378-8-49 |
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