Effect of thermotolerance on heat-induced excess nuclear-associated proteins
Earlier studies reported that thermotolerance had two effects on the heat‐induced increase in nuclear‐associated proteins (NAPs); reduction in NAP levels immediately following hyperthermia and facilitation of NAP recovery to control levels. It has also been demonstrated that there are two phases of...
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Veröffentlicht in: | Journal of cellular physiology 1993-07, Vol.156 (1), p.171-181 |
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description | Earlier studies reported that thermotolerance had two effects on the heat‐induced increase in nuclear‐associated proteins (NAPs); reduction in NAP levels immediately following hyperthermia and facilitation of NAP recovery to control levels. It has also been demonstrated that there are two phases of thermotolerance; one that requires newly synthesized proteins (protein synthesis dependent thermotolerance; PSDT), and another that does not (protein synthesis independent thermotolerance; PSIT). This study was designed to determine if these two phases of thermotolerance affected NAP binding in a similar or different manner. The results demonstrated that protein synthesis during thermotolerance development was not required to reduce NAP levels measured immediately following hyperthermia, but was required to facilitate NAP recovery to control levels following hyperthermia. Reducing NAP levels was the predominant mechanism by which thermotolerance protected cells from this lesion at 43.0°C while facilitated NAP recovery predominated in protecting against exposure to 45.5°C. The facilitated recovery of NAPs required only proteins synthesized following thermotolerance induction and prior to the second heat challenge. Proteins synthesized following the second heat challenge were not requisite. Finally, the processes that facilitate NAP recovery were inhibited at 3°C, suggesting that they are enzymatically mediated. © 1993 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/jcp.1041560123 |
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It has also been demonstrated that there are two phases of thermotolerance; one that requires newly synthesized proteins (protein synthesis dependent thermotolerance; PSDT), and another that does not (protein synthesis independent thermotolerance; PSIT). This study was designed to determine if these two phases of thermotolerance affected NAP binding in a similar or different manner. The results demonstrated that protein synthesis during thermotolerance development was not required to reduce NAP levels measured immediately following hyperthermia, but was required to facilitate NAP recovery to control levels following hyperthermia. Reducing NAP levels was the predominant mechanism by which thermotolerance protected cells from this lesion at 43.0°C while facilitated NAP recovery predominated in protecting against exposure to 45.5°C. The facilitated recovery of NAPs required only proteins synthesized following thermotolerance induction and prior to the second heat challenge. Proteins synthesized following the second heat challenge were not requisite. Finally, the processes that facilitate NAP recovery were inhibited at 3°C, suggesting that they are enzymatically mediated. © 1993 Wiley‐Liss, Inc.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.1041560123</identifier><identifier>PMID: 8314856</identifier><identifier>CODEN: JCLLAX</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Biological and medical sciences ; Cell physiology ; Cell Survival ; CHO Cells ; Cricetinae ; Cycloheximide - pharmacology ; Effects of physical and chemical agents ; Fundamental and applied biological sciences. Psychology ; Heat-Shock Proteins - metabolism ; Hot Temperature ; In Vitro Techniques ; Molecular and cellular biology ; Nuclear Proteins - biosynthesis ; Nuclear Proteins - metabolism ; Time Factors</subject><ispartof>Journal of cellular physiology, 1993-07, Vol.156 (1), p.171-181</ispartof><rights>Copyright © 1993 Wiley‐Liss, Inc.</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4073-8d400923e20b5a8fdc7765ffde08dd88c32db19217dbd41c6e0955016e8e4a573</citedby><cites>FETCH-LOGICAL-c4073-8d400923e20b5a8fdc7765ffde08dd88c32db19217dbd41c6e0955016e8e4a573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.1041560123$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.1041560123$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4857908$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8314856$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Borrelli, Michael J.</creatorcontrib><creatorcontrib>Stafford, Diane M.</creatorcontrib><creatorcontrib>Rausch, Cynthia M.</creatorcontrib><creatorcontrib>Lee, Yong J.</creatorcontrib><creatorcontrib>Corry, Peter M.</creatorcontrib><title>Effect of thermotolerance on heat-induced excess nuclear-associated proteins</title><title>Journal of cellular physiology</title><addtitle>J. Cell. Physiol</addtitle><description>Earlier studies reported that thermotolerance had two effects on the heat‐induced increase in nuclear‐associated proteins (NAPs); reduction in NAP levels immediately following hyperthermia and facilitation of NAP recovery to control levels. It has also been demonstrated that there are two phases of thermotolerance; one that requires newly synthesized proteins (protein synthesis dependent thermotolerance; PSDT), and another that does not (protein synthesis independent thermotolerance; PSIT). This study was designed to determine if these two phases of thermotolerance affected NAP binding in a similar or different manner. The results demonstrated that protein synthesis during thermotolerance development was not required to reduce NAP levels measured immediately following hyperthermia, but was required to facilitate NAP recovery to control levels following hyperthermia. Reducing NAP levels was the predominant mechanism by which thermotolerance protected cells from this lesion at 43.0°C while facilitated NAP recovery predominated in protecting against exposure to 45.5°C. The facilitated recovery of NAPs required only proteins synthesized following thermotolerance induction and prior to the second heat challenge. Proteins synthesized following the second heat challenge were not requisite. Finally, the processes that facilitate NAP recovery were inhibited at 3°C, suggesting that they are enzymatically mediated. © 1993 Wiley‐Liss, Inc.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell physiology</subject><subject>Cell Survival</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>Cycloheximide - pharmacology</subject><subject>Effects of physical and chemical agents</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>Hot Temperature</subject><subject>In Vitro Techniques</subject><subject>Molecular and cellular biology</subject><subject>Nuclear Proteins - biosynthesis</subject><subject>Nuclear Proteins - metabolism</subject><subject>Time Factors</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtLAzEURoMoWh9bd8IsxN1oMnnOUkutSvGBiuAmpMkNjk5najKD-u-NtFRcuUrgO9-9l4PQPsHHBOPi5NXO04cRLjAp6BoaEFzKnAlerKNBAkhecka20HaMrxjjsqR0E20qSpjiYoAmI-_Bdlnrs-4Fwqzt2hqCaSxkbZO9gOnyqnG9BZfBp4UYs6a3NZiQmxhbW5kuJfPQdlA1cRdteFNH2Fu-O-jxfPQwvMgnN-PL4ekktwxLmivH0iEFhQJPuVHeWSkF994BVs4pZWnhpqQsiHRTx4gVgEvOMRGggBku6Q46WsxNi997iJ2eVdFCXZsG2j5qyRUWgrAEHi9AG9oYA3g9D9XMhC9NsP7Rp5M-_asvFQ6Wk_vpDNwKX_pK-eEyN9Ga2v-YquIKS4wssUpYucA-qhq-_lmqr4a3f07IF90qdvC56prwpoWkkuun67G-untmw7N7psf0Gw09l64</recordid><startdate>199307</startdate><enddate>199307</enddate><creator>Borrelli, Michael J.</creator><creator>Stafford, Diane M.</creator><creator>Rausch, Cynthia M.</creator><creator>Lee, Yong J.</creator><creator>Corry, Peter M.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>199307</creationdate><title>Effect of thermotolerance on heat-induced excess nuclear-associated proteins</title><author>Borrelli, Michael J. ; Stafford, Diane M. ; Rausch, Cynthia M. ; Lee, Yong J. ; Corry, Peter M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4073-8d400923e20b5a8fdc7765ffde08dd88c32db19217dbd41c6e0955016e8e4a573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell physiology</topic><topic>Cell Survival</topic><topic>CHO Cells</topic><topic>Cricetinae</topic><topic>Cycloheximide - pharmacology</topic><topic>Effects of physical and chemical agents</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heat-Shock Proteins - metabolism</topic><topic>Hot Temperature</topic><topic>In Vitro Techniques</topic><topic>Molecular and cellular biology</topic><topic>Nuclear Proteins - biosynthesis</topic><topic>Nuclear Proteins - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Borrelli, Michael J.</creatorcontrib><creatorcontrib>Stafford, Diane M.</creatorcontrib><creatorcontrib>Rausch, Cynthia M.</creatorcontrib><creatorcontrib>Lee, Yong J.</creatorcontrib><creatorcontrib>Corry, Peter M.</creatorcontrib><collection>Istex</collection><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>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Borrelli, Michael J.</au><au>Stafford, Diane M.</au><au>Rausch, Cynthia M.</au><au>Lee, Yong J.</au><au>Corry, Peter M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of thermotolerance on heat-induced excess nuclear-associated proteins</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J. Cell. Physiol</addtitle><date>1993-07</date><risdate>1993</risdate><volume>156</volume><issue>1</issue><spage>171</spage><epage>181</epage><pages>171-181</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><coden>JCLLAX</coden><abstract>Earlier studies reported that thermotolerance had two effects on the heat‐induced increase in nuclear‐associated proteins (NAPs); reduction in NAP levels immediately following hyperthermia and facilitation of NAP recovery to control levels. It has also been demonstrated that there are two phases of thermotolerance; one that requires newly synthesized proteins (protein synthesis dependent thermotolerance; PSDT), and another that does not (protein synthesis independent thermotolerance; PSIT). This study was designed to determine if these two phases of thermotolerance affected NAP binding in a similar or different manner. The results demonstrated that protein synthesis during thermotolerance development was not required to reduce NAP levels measured immediately following hyperthermia, but was required to facilitate NAP recovery to control levels following hyperthermia. Reducing NAP levels was the predominant mechanism by which thermotolerance protected cells from this lesion at 43.0°C while facilitated NAP recovery predominated in protecting against exposure to 45.5°C. The facilitated recovery of NAPs required only proteins synthesized following thermotolerance induction and prior to the second heat challenge. Proteins synthesized following the second heat challenge were not requisite. Finally, the processes that facilitate NAP recovery were inhibited at 3°C, suggesting that they are enzymatically mediated. © 1993 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>8314856</pmid><doi>10.1002/jcp.1041560123</doi><tpages>11</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Cell physiology Cell Survival CHO Cells Cricetinae Cycloheximide - pharmacology Effects of physical and chemical agents Fundamental and applied biological sciences. Psychology Heat-Shock Proteins - metabolism Hot Temperature In Vitro Techniques Molecular and cellular biology Nuclear Proteins - biosynthesis Nuclear Proteins - metabolism Time Factors |
title | Effect of thermotolerance on heat-induced excess nuclear-associated proteins |
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