<?xml version="1.0" encoding="utf-8"?>
<article article-type="research-article" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML">
    <front>
        <journal-meta>
            <journal-id journal-id-type="publisher-id">TOBIOJ</journal-id>
            <journal-title>The Open Biology Journal</journal-title>
            <abbrev-journal-title abbrev-type="pubmed">Open Biol. J.</abbrev-journal-title>
            <issn pub-type="epub">1874-1967</issn>
            <publisher>
                <publisher-name>Bentham Open</publisher-name>
            </publisher>
        </journal-meta>
        <article-meta>
            <article-id pub-id-type="publisher-id">TOBIOJ-4-10</article-id>
            <article-id pub-id-type="doi">10.2174/1874196701104010010</article-id>
            <article-categories>
                <subj-group subj-group-type="heading">
                    <subject>Biology</subject>
                </subj-group>
            </article-categories>
            <title-group>
                <article-title>Protein Kinase-Regulated Inwardly Rectifying Anion and Organic Osmolyte Channels in Malaria-Infected Erythrocytes</article-title>
            </title-group>
            <contrib-group>
                <contrib contrib-type="author">
                    <name>
                        <surname>Bouyer</surname>
                        <given-names>Guillaume</given-names>
                    </name>
                </contrib>
                <contrib contrib-type="author">
                    <name>
                        <surname>L.Y. Thomas</surname>
                        <given-names>Serge</given-names>
                    </name>
                </contrib>
                <contrib contrib-type="author" corresp="yes">
                    <name>
                        <surname>Eg&#xE9;e</surname>
                        <given-names>St&#xE9;phane</given-names>
                    </name>
                    <xref ref-type="corresp" rid="cor1">&#x002A;</xref>
                    <xref ref-type="aff" rid="aff1">1</xref>
                    <xref ref-type="aff" rid="aff2">2</xref>
                    <xref ref-type="aff" rid="aff3">3</xref>
                </contrib>
            </contrib-group>
            <aff id="aff1">
                <label>1</label>Université Pierre et Marie Curie, UMR 7150, Equipe Physiologie Comparée des Erythrocytes, Station Biologique, B.
P. 74, 29682 Roscoff cedex, France</aff>
            <aff id="aff2">
                <label>2</label>Centre National de la Recherche Scientifique, UMR 7150, Equipe Physiologie Comparée des Erythrocytes, Station
Biologique, B. P. 74, 29682 Roscoff cedex, France</aff>
            <aff id="aff3">
                <label>3</label>Université Européenne de Bretagne, UMR 7150, Equipe Physiologie Comparée des Erythrocytes, Station Biologique,
B. P. 74, 29682 Roscoff cedex, France</aff>
            <author-notes>
                <corresp id="cor1">
                    <label>&#x002A;</label>Address correspondence to this author at the Université Pierre et Marie
Curie, UMR 7150, Equipe Physiologie Comparée des Erythrocytes, Station
Biologique, B. P. 74, 29682 Roscoff cedex, France; Tel: (33) 02 98 29 23
82; E-mail: <email xlink:href="egee@sb-roscoff.fr">egee@sb-roscoff.fr</email></corresp>
            </author-notes>
            <pub-date pub-type="epub">
                <day>31</day>
                <month>01</month>
                <year>2011</year>
            </pub-date>
            <pub-date pub-type="collection">
                <year>2011</year>
            </pub-date>
            <volume>04</volume>
            <fpage>10</fpage>
            <lpage>17</lpage>
            <history>
                <date date-type="received">
                    <day>20</day>
                    <month>09</month>
                    <year>2009</year>
                </date>
                <date date-type="rev-recd">
                    <day>15</day>
                    <month>03</month>
                    <year>2010</year>
                </date>
                <date date-type="accepted">
                    <day>16</day>
                    <month>03</month>
                    <year>2010</year>
                </date>
            </history>
            <permissions>
                <copyright-statement>&#x00A9; 2010 Bouyer <italic>et al</italic>.</copyright-statement>
                <copyright-year>2011</copyright-year>
                <copyright-holder>Guillaume Bouyer</copyright-holder>
                <license license-type="open-access" xlink:href="https://creativecommons.org/licenses/by/4.0/legalcode">
                    <p>This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: <uri xlink:href="https://creativecommons.org/licenses/by/4.0/legalcode">https://creativecommons.org/licenses/by/4.0/legalcode</uri>.  This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</p>
                </license>
            </permissions>
            <abstract>
                <p>The intraerythrocytic amplification of the malaria parasite Plasmodium falciparum induces new pathways of
solute permeability in the host cell's membrane. These pathways play a pivotal role in parasite development by supplying
the parasite with nutrients, disposing of the parasite's metabolic waste and organic osmolytes, and adapting the host's
electrolyte composition to the parasite's needs. During the last ten years, electrophysiological investigations strongly
supported earlier evidence obtained by transport and pharmacological studies that this new permeability pathway, which
is induced by the parasite in the host cell membrane, is constituted by anion-selective channels. This review surveys the
evidences acquired using the patch-clamp technique and discuss the hypothesis that protein kinase A is an effector of the
signalling pathway leading to the activation of endogenous channels upon infection.</p>
            </abstract>
            <kwd-group>
                <title>Keywords</title>
                <kwd>Erythrocyte</kwd>
                <kwd>
                    <italic>Plasmodium</italic>
                </kwd>
                <kwd>new permeation pathways</kwd>
                <kwd>protein kinase A</kwd>
                <kwd>ion channel</kwd>
            </kwd-group>
        </article-meta>
    </front>
</article>
