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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">TRPM7, the cytoskeleton and neuronal death</title><author><name sortKey="Asrar, Suhail" sort="Asrar, Suhail" uniqKey="Asrar S" first="Suhail" last="Asrar">Suhail Asrar</name></author><author><name sortKey="Aarts, Michelle" sort="Aarts, Michelle" uniqKey="Aarts M" first="Michelle" last="Aarts">Michelle Aarts</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23247582</idno><idno type="pmc">3589284</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3589284</idno><idno type="RBID">PMC:3589284</idno><idno type="doi">10.4161/chan.22824</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000B77</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000B77</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">TRPM7, the cytoskeleton and neuronal death</title><author><name sortKey="Asrar, Suhail" sort="Asrar, Suhail" uniqKey="Asrar S" first="Suhail" last="Asrar">Suhail Asrar</name></author><author><name sortKey="Aarts, Michelle" sort="Aarts, Michelle" uniqKey="Aarts M" first="Michelle" last="Aarts">Michelle Aarts</name></author></analytic><series><title level="j">Channels</title><idno type="ISSN">1933-6950</idno><idno type="eISSN">1933-6969</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Ischemic stroke is one of the leading causes of disability and death in the world. Elucidation of the underlying mechanisms associated with neuronal death during this detrimental process has been of significant interest in the field of research. One principle component vital to the maintenance of cellular integrity is the cytoskeleton. Studies suggest that abnormalities at the level of this fundamental structure are directly linked to adverse effects on cellular well-being, including cell death. In recent years, evidence has also emerged regarding an imperative role for the transient receptor potential (TRP) family member TRPM7 in the mediation of excitotoxic-independent neuronal demise. In this review, we will elaborate on the current knowledge and unique properties associated with the functioning of this structure. In addition, we will deliberate the involvement of distinct mechanistic pathways during TRPM7-dependent cell death, including modifications at the level of the cytoskeleton.</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">Channels (Austin)</journal-id><journal-id journal-id-type="iso-abbrev">Channels (Austin)</journal-id><journal-id journal-id-type="publisher-id">CHAN</journal-id><journal-title-group><journal-title>Channels</journal-title></journal-title-group><issn pub-type="ppub">1933-6950</issn><issn pub-type="epub">1933-6969</issn><publisher><publisher-name>Landes Bioscience</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23247582</article-id><article-id pub-id-type="pmc">3589284</article-id><article-id pub-id-type="publisher-id">2012CHANNELS0090R</article-id><article-id pub-id-type="doi">10.4161/chan.22824</article-id><article-id pub-id-type="pii">22824</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>TRPM7, the cytoskeleton and neuronal death</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Asrar</surname><given-names>Suhail</given-names></name></contrib><contrib contrib-type="author"><name><surname>Aarts</surname><given-names>Michelle</given-names></name><xref ref-type="corresp" rid="cor1">*</xref></contrib><aff id="A1">Department of Biological Sciences; University of Toronto; Scarborough, ON Canada</aff></contrib-group><author-notes><corresp id="cor1"><bold>* Correspondence to:</bold> Michelle Aarts; Email: <email xlink:href="maarts@utsc.utoronto.ca">maarts@utsc.utoronto.ca</email></corresp></author-notes><pub-date pub-type="ppub"><day>01</day><month>1</month><year>2013</year></pub-date><volume>7</volume><issue>1</issue><fpage>6</fpage><lpage>16</lpage><permissions><copyright-statement>Copyright © 2013 Landes Bioscience</copyright-statement><copyright-year>2013</copyright-year></permissions><abstract><p>Ischemic stroke is one of the leading causes of disability and death in the world. Elucidation of the underlying mechanisms associated with neuronal death during this detrimental process has been of significant interest in the field of research. One principle component vital to the maintenance of cellular integrity is the cytoskeleton. Studies suggest that abnormalities at the level of this fundamental structure are directly linked to adverse effects on cellular well-being, including cell death. In recent years, evidence has also emerged regarding an imperative role for the transient receptor potential (TRP) family member TRPM7 in the mediation of excitotoxic-independent neuronal demise. In this review, we will elaborate on the current knowledge and unique properties associated with the functioning of this structure. In addition, we will deliberate the involvement of distinct mechanistic pathways during TRPM7-dependent cell death, including modifications at the level of the cytoskeleton.</p></abstract><kwd-group kwd-group-type="author"><title>Keywords: </title><kwd>TRPM7</kwd><kwd>cytoskeleton</kwd><kwd>calcium</kwd><kwd>ischemia</kwd><kwd>neuron</kwd><kwd>stroke</kwd><kwd>OGD</kwd><kwd>cofilin</kwd><kwd>kinase</kwd><kwd>anoxia</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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