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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Rab GTPases implicated in inherited and acquired disorders</title><author><name sortKey="Mitra, Shreya" sort="Mitra, Shreya" uniqKey="Mitra S" first="Shreya" last="Mitra">Shreya Mitra</name></author><author><name sortKey="Cheng, Kwai W" sort="Cheng, Kwai W" uniqKey="Cheng K" first="Kwai W." last="Cheng">Kwai W. Cheng</name></author><author><name sortKey="Mills, Gordon B" sort="Mills, Gordon B" uniqKey="Mills G" first="Gordon B." last="Mills">Gordon B. Mills</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21147240</idno><idno type="pmc">3395236</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395236</idno><idno type="RBID">PMC:3395236</idno><idno type="doi">10.1016/j.semcdb.2010.12.005</idno><date when="2010">2010</date><idno type="wicri:Area/Pmc/Corpus">000270</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000270</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Rab GTPases implicated in inherited and acquired disorders</title><author><name sortKey="Mitra, Shreya" sort="Mitra, Shreya" uniqKey="Mitra S" first="Shreya" last="Mitra">Shreya Mitra</name></author><author><name sortKey="Cheng, Kwai W" sort="Cheng, Kwai W" uniqKey="Cheng K" first="Kwai W." last="Cheng">Kwai W. Cheng</name></author><author><name sortKey="Mills, Gordon B" sort="Mills, Gordon B" uniqKey="Mills G" first="Gordon B." last="Mills">Gordon B. Mills</name></author></analytic><series><title level="j">Seminars in cell & developmental biology</title><idno type="ISSN">1084-9521</idno><idno type="eISSN">1096-3634</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Endocytotic pathways ensure that internalized receptor complexes are routed in a highly orchestrated manner to the correct subcellular destinations. This, in turn, determines the consequences of receptor activation through targeting receptors and ligand for recycling or degradation as well as by the formation of signaling complexes within the cell that alter the kinetics and magnitude of activation of specific downstream signal transduction cascades. Thus the control of the fate of activated receptor complexes has profound physiologic and pathophysiologic implications. Rab GTPases, the largest subfamily of the RAS small GTPase superfamily, are the key regulators of endocytosis through decorating and targeting intracellular vesicles and cargoes to appropriate subcellular compartments. The six-fold increase in Rab family members from yeast to man correlates closely with the evolutionary increase in endomembrane complexity compatible with a rapid diversification of function of Rab GTPase decorated vesicles. As the vesicular cargo includes growth factors, nutrients, cytokines, integrins and even pathogens, aberrations in the pathway are likely to exhibit dire consequences. Several genetic diseases driven by mutations in Rab GTPases or their interacting proteins have been identified [<xref rid="R1" ref-type="bibr">1</xref>], [<xref rid="R2" ref-type="bibr">2</xref>], [<xref rid="R3" ref-type="bibr">3</xref>]. Aberrant Rab GTPase function has been implicated in diverse pathophysiologies including loss of hair, skin and eye pigmentation, loss of vision, loss of renal function, mental retardation, muscle skeletal degeneration, immune deficiency, infection, obesity, diabetes and cancer.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">9607332</journal-id><journal-id journal-id-type="pubmed-jr-id">20707</journal-id><journal-id journal-id-type="nlm-ta">Semin Cell Dev Biol</journal-id><journal-id journal-id-type="iso-abbrev">Semin. Cell Dev. Biol.</journal-id><journal-title-group><journal-title>Seminars in cell & developmental biology</journal-title></journal-title-group><issn pub-type="ppub">1084-9521</issn><issn pub-type="epub">1096-3634</issn></journal-meta><article-meta><article-id pub-id-type="pmid">21147240</article-id><article-id pub-id-type="pmc">3395236</article-id><article-id pub-id-type="doi">10.1016/j.semcdb.2010.12.005</article-id><article-id pub-id-type="manuscript">NIHMS384559</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Rab GTPases implicated in inherited and acquired disorders</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Mitra</surname><given-names>Shreya</given-names></name><xref rid="FN1" ref-type="author-notes">*</xref></contrib><contrib contrib-type="author"><name><surname>Cheng</surname><given-names>Kwai W.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Mills</surname><given-names>Gordon B.</given-names></name></contrib><aff id="A1">Department of Systems Biology, The University of Texas, MD Anderson Cancer Center 7435 Fannin St, Suite 2SCR3.1030, Houston, Texas- 77054-1942, USA</aff></contrib-group><author-notes><corresp id="FN1"><label>*</label>To whom correspondence should be addressed. <email>smitra@mdanderson.org</email>; Phone: 1-713-563-2848; Fax: 1-713-563-4235</corresp></author-notes><pub-date pub-type="nihms-submitted"><day>25</day><month>6</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>13</day><month>12</month><year>2010</year></pub-date><pub-date pub-type="ppub"><month>2</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>12</day><month>7</month><year>2012</year></pub-date><volume>22</volume><issue>1</issue><fpage>57</fpage><lpage>68</lpage><abstract><p id="P1">Endocytotic pathways ensure that internalized receptor complexes are routed in a highly orchestrated manner to the correct subcellular destinations. This, in turn, determines the consequences of receptor activation through targeting receptors and ligand for recycling or degradation as well as by the formation of signaling complexes within the cell that alter the kinetics and magnitude of activation of specific downstream signal transduction cascades. Thus the control of the fate of activated receptor complexes has profound physiologic and pathophysiologic implications. Rab GTPases, the largest subfamily of the RAS small GTPase superfamily, are the key regulators of endocytosis through decorating and targeting intracellular vesicles and cargoes to appropriate subcellular compartments. The six-fold increase in Rab family members from yeast to man correlates closely with the evolutionary increase in endomembrane complexity compatible with a rapid diversification of function of Rab GTPase decorated vesicles. As the vesicular cargo includes growth factors, nutrients, cytokines, integrins and even pathogens, aberrations in the pathway are likely to exhibit dire consequences. Several genetic diseases driven by mutations in Rab GTPases or their interacting proteins have been identified [<xref rid="R1" ref-type="bibr">1</xref>], [<xref rid="R2" ref-type="bibr">2</xref>], [<xref rid="R3" ref-type="bibr">3</xref>]. Aberrant Rab GTPase function has been implicated in diverse pathophysiologies including loss of hair, skin and eye pigmentation, loss of vision, loss of renal function, mental retardation, muscle skeletal degeneration, immune deficiency, infection, obesity, diabetes and cancer.</p></abstract><funding-group><award-group><funding-source country="United States">National Cancer Institute : NCI</funding-source><award-id>P30 CA016672 || CA</award-id></award-group><award-group><funding-source country="United States">National Cancer Institute : NCI</funding-source><award-id>P01 CA099031 || CA</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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