From oncogenic mutation to dynamic code
Oncogenic BRAF mutations can distort downstream signaling outcomes Signal transduction pathways (STPs) convert biochemical reactions into precise and reproducible biological outcomes. These functions are performed reliably and reproducibly against a background of noise (variation) arising from the s...
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Veröffentlicht in: | Science (American Association for the Advancement of Science) 2018-08, Vol.361 (6405), p.844-845 |
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creator | Kolch, Walter Kiel, Christina |
description | Oncogenic BRAF mutations can distort downstream signaling outcomes
Signal transduction pathways (STPs) convert biochemical reactions into precise and reproducible biological outcomes. These functions are performed reliably and reproducibly against a background of noise (variation) arising from the stochastic nature of biochemical reactions (
1
). Indeed, information theory analysis of STPs indicates that they have a limited capacity to discriminate information, including different ligands or different activation states of components (
2
). However, this discrimination is dramatically enhanced by adding dynamic information, such as signal rise time, signal duration, amplitude, and decay rate (
3
). The observation that differential activation dynamics of the extracellular signal-regulated kinase (ERK) pathway can determine whether rat pheochromocytoma cells proliferate or differentiate was reported more than 20 years ago (
4
), and evidence has since accumulated that STP dynamics control cell fate decisions. However, we are still struggling to understand how signaling dynamics is encoded and decoded and how pathological changes, such as the expression of mutant proteins, affect the dynamic STP code. On page 892 of this issue, Bugaj
et al.
(
5
) make use of new tools with which to decipher this code and reveal how certain cancer-associated BRAF mutations can corrupt the dynamic STP code and trick cells into unlicensed proliferation. |
doi_str_mv | 10.1126/science.aau8059 |
format | Article |
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Signal transduction pathways (STPs) convert biochemical reactions into precise and reproducible biological outcomes. These functions are performed reliably and reproducibly against a background of noise (variation) arising from the stochastic nature of biochemical reactions (
1
). Indeed, information theory analysis of STPs indicates that they have a limited capacity to discriminate information, including different ligands or different activation states of components (
2
). However, this discrimination is dramatically enhanced by adding dynamic information, such as signal rise time, signal duration, amplitude, and decay rate (
3
). The observation that differential activation dynamics of the extracellular signal-regulated kinase (ERK) pathway can determine whether rat pheochromocytoma cells proliferate or differentiate was reported more than 20 years ago (
4
), and evidence has since accumulated that STP dynamics control cell fate decisions. However, we are still struggling to understand how signaling dynamics is encoded and decoded and how pathological changes, such as the expression of mutant proteins, affect the dynamic STP code. On page 892 of this issue, Bugaj
et al.
(
5
) make use of new tools with which to decipher this code and reveal how certain cancer-associated BRAF mutations can corrupt the dynamic STP code and trick cells into unlicensed proliferation.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.aau8059</identifier><identifier>PMID: 30166473</identifier><language>eng</language><publisher>United States: The American Association for the Advancement of Science</publisher><subject>Activation ; Background noise ; Cancer ; Cell fate ; Cell proliferation ; Coding ; Decay rate ; Extracellular signal-regulated kinase ; Genetic Code ; Information theory ; Metabolic pathways ; Mutation ; Pheochromocytoma cells ; Proteins ; Signal transduction ; Stochasticity</subject><ispartof>Science (American Association for the Advancement of Science), 2018-08, Vol.361 (6405), p.844-845</ispartof><rights>Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c325t-61de8636d33ecb84fe399a716a766ef74706e1ffbeafd65b6b0be1ea8c19e3823</citedby><cites>FETCH-LOGICAL-c325t-61de8636d33ecb84fe399a716a766ef74706e1ffbeafd65b6b0be1ea8c19e3823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2884,2885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30166473$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kolch, Walter</creatorcontrib><creatorcontrib>Kiel, Christina</creatorcontrib><title>From oncogenic mutation to dynamic code</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Oncogenic BRAF mutations can distort downstream signaling outcomes
Signal transduction pathways (STPs) convert biochemical reactions into precise and reproducible biological outcomes. These functions are performed reliably and reproducibly against a background of noise (variation) arising from the stochastic nature of biochemical reactions (
1
). Indeed, information theory analysis of STPs indicates that they have a limited capacity to discriminate information, including different ligands or different activation states of components (
2
). However, this discrimination is dramatically enhanced by adding dynamic information, such as signal rise time, signal duration, amplitude, and decay rate (
3
). The observation that differential activation dynamics of the extracellular signal-regulated kinase (ERK) pathway can determine whether rat pheochromocytoma cells proliferate or differentiate was reported more than 20 years ago (
4
), and evidence has since accumulated that STP dynamics control cell fate decisions. However, we are still struggling to understand how signaling dynamics is encoded and decoded and how pathological changes, such as the expression of mutant proteins, affect the dynamic STP code. On page 892 of this issue, Bugaj
et al.
(
5
) make use of new tools with which to decipher this code and reveal how certain cancer-associated BRAF mutations can corrupt the dynamic STP code and trick cells into unlicensed proliferation.</description><subject>Activation</subject><subject>Background noise</subject><subject>Cancer</subject><subject>Cell fate</subject><subject>Cell proliferation</subject><subject>Coding</subject><subject>Decay rate</subject><subject>Extracellular signal-regulated kinase</subject><subject>Genetic Code</subject><subject>Information theory</subject><subject>Metabolic pathways</subject><subject>Mutation</subject><subject>Pheochromocytoma cells</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Stochasticity</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkDFPwzAQRi0EoqEws6FIDLCkPecSOx5RRQGpEgvMluNcUKomLnYy9N-TqoGB6aS7d58-PcZuOSw4T8Uy2IY6SwtjhgJydcYiDipPVAp4ziIAFEkBMp-xqxC2AONN4SWbIXAhMokRe1h718aus-6LusbG7dCbvnFd3Lu4OnSmHXfWVXTNLmqzC3QzzTn7XD9_rF6TzfvL2-ppk1hM8z4RvKJCoKgQyZZFVhMqZSQXRgpBtcwkCOJ1XZKpK5GXooSSOJnCckVYpDhnj6fcvXffA4Vet02wtNuZjtwQdAqqkBIy5CN6_w_dusF3Y7sjJccWUsBILU-U9S4ET7Xe-6Y1_qA56KNDPTnUk8Px427KHcqWqj_-Vxr-AL5ibec</recordid><startdate>20180831</startdate><enddate>20180831</enddate><creator>Kolch, Walter</creator><creator>Kiel, Christina</creator><general>The American Association for the Advancement of Science</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QF</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QQ</scope><scope>7QR</scope><scope>7SC</scope><scope>7SE</scope><scope>7SN</scope><scope>7SP</scope><scope>7SR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7TK</scope><scope>7TM</scope><scope>7U5</scope><scope>7U9</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>H94</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20180831</creationdate><title>From oncogenic mutation to dynamic code</title><author>Kolch, Walter ; 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Signal transduction pathways (STPs) convert biochemical reactions into precise and reproducible biological outcomes. These functions are performed reliably and reproducibly against a background of noise (variation) arising from the stochastic nature of biochemical reactions (
1
). Indeed, information theory analysis of STPs indicates that they have a limited capacity to discriminate information, including different ligands or different activation states of components (
2
). However, this discrimination is dramatically enhanced by adding dynamic information, such as signal rise time, signal duration, amplitude, and decay rate (
3
). The observation that differential activation dynamics of the extracellular signal-regulated kinase (ERK) pathway can determine whether rat pheochromocytoma cells proliferate or differentiate was reported more than 20 years ago (
4
), and evidence has since accumulated that STP dynamics control cell fate decisions. However, we are still struggling to understand how signaling dynamics is encoded and decoded and how pathological changes, such as the expression of mutant proteins, affect the dynamic STP code. On page 892 of this issue, Bugaj
et al.
(
5
) make use of new tools with which to decipher this code and reveal how certain cancer-associated BRAF mutations can corrupt the dynamic STP code and trick cells into unlicensed proliferation.</abstract><cop>United States</cop><pub>The American Association for the Advancement of Science</pub><pmid>30166473</pmid><doi>10.1126/science.aau8059</doi><tpages>2</tpages></addata></record> |
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subjects | Activation Background noise Cancer Cell fate Cell proliferation Coding Decay rate Extracellular signal-regulated kinase Genetic Code Information theory Metabolic pathways Mutation Pheochromocytoma cells Proteins Signal transduction Stochasticity |
title | From oncogenic mutation to dynamic code |
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