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Insulin Receptor Substrate Regulation of Phosphoinositide 3-Kinase
Insulin receptor substrates (IRS) serve as downstream messengers from activated cell surface receptors to numerous signaling pathway cascades. One of these pathways, phosphoinositide 3-kinase (PI3K), frequently displays aberrant function in the setting of cancer. IRS proteins are capable of both reg...
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Published in: | Clinical cancer research 2011-01, Vol.17 (2), p.206-211 |
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container_title | Clinical cancer research |
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creator | METZ, Heather E MCGARRY HOUGHTON, A |
description | Insulin receptor substrates (IRS) serve as downstream messengers from activated cell surface receptors to numerous signaling pathway cascades. One of these pathways, phosphoinositide 3-kinase (PI3K), frequently displays aberrant function in the setting of cancer. IRS proteins are capable of both regulating and activating PI3K, depending on the cell of origin. As such, both prohost and protumor functions have been described for IRS proteins in human cancers. IRS proteins may eventually serve as biomarkers of PI3K activity, and serve a much-needed role as a guide to using targeted pathway therapy. Additionally, IRS-1 could be indirectly targeted in lung cancer, by inhibiting neutrophil elastase, which functions to degrade IRS-1 in lung tumor cells, thereby generating PI3K hyperactivity. |
doi_str_mv | 10.1158/1078-0432.ccr-10-0434 |
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One of these pathways, phosphoinositide 3-kinase (PI3K), frequently displays aberrant function in the setting of cancer. IRS proteins are capable of both regulating and activating PI3K, depending on the cell of origin. As such, both prohost and protumor functions have been described for IRS proteins in human cancers. IRS proteins may eventually serve as biomarkers of PI3K activity, and serve a much-needed role as a guide to using targeted pathway therapy. Additionally, IRS-1 could be indirectly targeted in lung cancer, by inhibiting neutrophil elastase, which functions to degrade IRS-1 in lung tumor cells, thereby generating PI3K hyperactivity.</description><subject>1-Phosphatidylinositol 4-Kinase - metabolism</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Insulin Receptor Substrate Proteins - physiology</subject><subject>Leukocyte Elastase - metabolism</subject><subject>Medical sciences</subject><subject>Neoplasms - metabolism</subject><subject>Pharmacology. 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Drug treatments</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>METZ, Heather E</creatorcontrib><creatorcontrib>MCGARRY HOUGHTON, A</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>METZ, Heather E</au><au>MCGARRY HOUGHTON, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin Receptor Substrate Regulation of Phosphoinositide 3-Kinase</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2011-01-15</date><risdate>2011</risdate><volume>17</volume><issue>2</issue><spage>206</spage><epage>211</epage><pages>206-211</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><coden>CCREF4</coden><abstract>Insulin receptor substrates (IRS) serve as downstream messengers from activated cell surface receptors to numerous signaling pathway cascades. 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source | Freely Accessible Science Journals |
subjects | 1-Phosphatidylinositol 4-Kinase - metabolism Antineoplastic agents Biological and medical sciences Gene Expression Regulation Humans Insulin Receptor Substrate Proteins - physiology Leukocyte Elastase - metabolism Medical sciences Neoplasms - metabolism Pharmacology. Drug treatments Signal Transduction |
title | Insulin Receptor Substrate Regulation of Phosphoinositide 3-Kinase |
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