Proline Mechanisms of Stress Survival
Identifieur interne : 000388 ( Ncbi/Merge ); précédent : 000387; suivant : 000389Proline Mechanisms of Stress Survival
Auteurs : Xinwen Liang ; Lu Zhang ; Sathish Kumar Natarajan ; Donald F. BeckerSource :
- Antioxidants & Redox Signaling [ 1523-0864 ] ; 2013.
Abstract
Url:
DOI: 10.1089/ars.2012.5074
PubMed: 23581681
PubMed Central: 3763223
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PMC:3763223Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Proline Mechanisms of Stress Survival</title>
<author><name sortKey="Liang, Xinwen" sort="Liang, Xinwen" uniqKey="Liang X" first="Xinwen" last="Liang">Xinwen Liang</name>
</author>
<author><name sortKey="Zhang, Lu" sort="Zhang, Lu" uniqKey="Zhang L" first="Lu" last="Zhang">Lu Zhang</name>
</author>
<author><name sortKey="Natarajan, Sathish Kumar" sort="Natarajan, Sathish Kumar" uniqKey="Natarajan S" first="Sathish Kumar" last="Natarajan">Sathish Kumar Natarajan</name>
</author>
<author><name sortKey="Becker, Donald F" sort="Becker, Donald F" uniqKey="Becker D" first="Donald F." last="Becker">Donald F. Becker</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Proline Mechanisms of Stress Survival</title>
<author><name sortKey="Liang, Xinwen" sort="Liang, Xinwen" uniqKey="Liang X" first="Xinwen" last="Liang">Xinwen Liang</name>
</author>
<author><name sortKey="Zhang, Lu" sort="Zhang, Lu" uniqKey="Zhang L" first="Lu" last="Zhang">Lu Zhang</name>
</author>
<author><name sortKey="Natarajan, Sathish Kumar" sort="Natarajan, Sathish Kumar" uniqKey="Natarajan S" first="Sathish Kumar" last="Natarajan">Sathish Kumar Natarajan</name>
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<author><name sortKey="Becker, Donald F" sort="Becker, Donald F" uniqKey="Becker D" first="Donald F." last="Becker">Donald F. Becker</name>
</author>
</analytic>
<series><title level="j">Antioxidants & Redox Signaling</title>
<idno type="ISSN">1523-0864</idno>
<idno type="eISSN">1557-7716</idno>
<imprint><date when="2013">2013</date>
</imprint>
</series>
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<front><div type="abstract" xml:lang="en"><title>Abstract</title>
<p><bold><italic>Significance:</italic>
</bold>
The imino acid proline is utilized by different organisms to offset cellular imbalances caused by environmental stress. The wide use in nature of proline as a stress adaptor molecule indicates that proline has a fundamental biological role in stress response. Understanding the mechanisms by which proline enhances abiotic/biotic stress response will facilitate agricultural crop research and improve human health. <bold><italic>Recent Advances</italic>
:</bold>
It is now recognized that proline metabolism propels cellular signaling processes that promote cellular apoptosis or survival. Studies have shown that proline metabolism influences signaling pathways by increasing reactive oxygen species (ROS) formation in the mitochondria <italic>via</italic>
the electron transport chain. Enhanced ROS production due to proline metabolism has been implicated in the hypersensitive response in plants, lifespan extension in worms, and apoptosis, tumor suppression, and cell survival in animals. <bold><italic>Critical Issues</italic>
:</bold>
The ability of proline to influence disparate cellular outcomes may be governed by ROS levels generated in the mitochondria. Defining the threshold at which proline metabolic enzyme expression switches from inducing survival pathways to cellular apoptosis would provide molecular insights into cellular redox regulation by proline. Are ROS the only mediators of proline metabolic signaling or are other factors involved? <bold><italic>Future Directions</italic>
:</bold>
New evidence suggests that proline biosynthesis enzymes interact with redox proteins such as thioredoxin. An important future pursuit will be to identify other interacting partners of proline metabolic enzymes to uncover novel regulatory and signaling networks of cellular stress response. <italic>Antioxid. Redox Signal</italic>
. 19, 998–1011.</p>
</div>
</front>
</TEI>
<pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Antioxid Redox Signal</journal-id>
<journal-id journal-id-type="iso-abbrev">Antioxid. Redox Signal</journal-id>
<journal-id journal-id-type="publisher-id">ars</journal-id>
<journal-title-group><journal-title>Antioxidants & Redox Signaling</journal-title>
</journal-title-group>
<issn pub-type="ppub">1523-0864</issn>
<issn pub-type="epub">1557-7716</issn>
<publisher><publisher-name>Mary Ann Liebert, Inc.</publisher-name>
<publisher-loc>140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">23581681</article-id>
<article-id pub-id-type="pmc">3763223</article-id>
<article-id pub-id-type="publisher-id">10.1089/ars.2012.5074</article-id>
<article-id pub-id-type="doi">10.1089/ars.2012.5074</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Forum Review Articles<break></break>
<italic>Plant Redox (M. Dickman, Ed.)</italic>
</subject>
</subj-group>
</article-categories>
<title-group><article-title>Proline Mechanisms of Stress Survival</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Liang</surname>
<given-names>Xinwen</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Lu</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Natarajan</surname>
<given-names>Sathish Kumar</given-names>
</name>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Becker</surname>
<given-names>Donald F.</given-names>
</name>
</contrib>
<aff id="aff1">Department of Biochemistry,<institution>University of Nebraska-Lincoln</institution>
, Lincoln, Nebraska.</aff>
</contrib-group>
<author-notes><corresp>Address correspondence to: <italic>Dr. Donald F. Becker, Department of Biochemistry, University of Nebraska-Lincoln, Lincoln, NE 68588-0664. E-mail:</italic>
<email xlink:href="mailto:dbecker3@unl.edu">dbecker3@unl.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><day>20</day>
<month>9</month>
<year>2013</year>
<pmc-comment>string-date: September 20, 2013</pmc-comment>
</pub-date>
<volume>19</volume>
<issue>9</issue>
<fpage>998</fpage>
<lpage>1011</lpage>
<history><date date-type="received"><day>06</day>
<month>11</month>
<year>2012</year>
<pmc-comment>string-date: Date of first submission to ARS Central, November 6, 2012</pmc-comment>
</date>
<date date-type="rev-recd"><day>22</day>
<month>3</month>
<year>2013</year>
<pmc-comment>string-date: date of final revised submission, March 22, 2013</pmc-comment>
</date>
<date date-type="accepted"><day>14</day>
<month>4</month>
<year>2013</year>
<pmc-comment>string-date: date of acceptance, April 14, 2013</pmc-comment>
</date>
</history>
<permissions><copyright-statement>Copyright 2013, Mary Ann Liebert, Inc.</copyright-statement>
<copyright-year>2013</copyright-year>
</permissions>
<self-uri xlink:type="simple" xlink:href="ars.2012.5074.pdf"></self-uri>
<abstract><title>Abstract</title>
<p><bold><italic>Significance:</italic>
</bold>
The imino acid proline is utilized by different organisms to offset cellular imbalances caused by environmental stress. The wide use in nature of proline as a stress adaptor molecule indicates that proline has a fundamental biological role in stress response. Understanding the mechanisms by which proline enhances abiotic/biotic stress response will facilitate agricultural crop research and improve human health. <bold><italic>Recent Advances</italic>
:</bold>
It is now recognized that proline metabolism propels cellular signaling processes that promote cellular apoptosis or survival. Studies have shown that proline metabolism influences signaling pathways by increasing reactive oxygen species (ROS) formation in the mitochondria <italic>via</italic>
the electron transport chain. Enhanced ROS production due to proline metabolism has been implicated in the hypersensitive response in plants, lifespan extension in worms, and apoptosis, tumor suppression, and cell survival in animals. <bold><italic>Critical Issues</italic>
:</bold>
The ability of proline to influence disparate cellular outcomes may be governed by ROS levels generated in the mitochondria. Defining the threshold at which proline metabolic enzyme expression switches from inducing survival pathways to cellular apoptosis would provide molecular insights into cellular redox regulation by proline. Are ROS the only mediators of proline metabolic signaling or are other factors involved? <bold><italic>Future Directions</italic>
:</bold>
New evidence suggests that proline biosynthesis enzymes interact with redox proteins such as thioredoxin. An important future pursuit will be to identify other interacting partners of proline metabolic enzymes to uncover novel regulatory and signaling networks of cellular stress response. <italic>Antioxid. Redox Signal</italic>
. 19, 998–1011.</p>
</abstract>
<counts><fig-count count="6"></fig-count>
<ref-count count="156"></ref-count>
<page-count count="14"></page-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Becker, Donald F" sort="Becker, Donald F" uniqKey="Becker D" first="Donald F." last="Becker">Donald F. Becker</name>
<name sortKey="Liang, Xinwen" sort="Liang, Xinwen" uniqKey="Liang X" first="Xinwen" last="Liang">Xinwen Liang</name>
<name sortKey="Natarajan, Sathish Kumar" sort="Natarajan, Sathish Kumar" uniqKey="Natarajan S" first="Sathish Kumar" last="Natarajan">Sathish Kumar Natarajan</name>
<name sortKey="Zhang, Lu" sort="Zhang, Lu" uniqKey="Zhang L" first="Lu" last="Zhang">Lu Zhang</name>
</noCountry>
</tree>
</affiliations>
</record>
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