InsP3 Signaling in Apicomplexan Parasites

Lade...
Vorschaubild
Dateien
Zu diesem Dokument gibt es keine Dateien.
Datum
2017
Autor:innen
Garcia, Celia R.S.
Alves, Eduardo
Pereira, Pedro H.S.
Bartlett, Paula
Thomas, Andrew
Mikoshiba, Katsuhiko
Sibley, L. David
Herausgeber:innen
Kontakt
ISSN der Zeitschrift
Electronic ISSN
ISBN
Bibliografische Daten
Verlag
Schriftenreihe
Auflagebezeichnung
URI (zitierfähiger Link)
ArXiv-ID
Internationale Patentnummer
EU-Projektnummer
DFG-Projektnummer
Projekt
Open Access-Veröffentlichung
Sammlungen
Gesperrt bis
Titel in einer weiteren Sprache
Forschungsvorhaben
Organisationseinheiten
Zeitschriftenheft
Publikationstyp
Zeitschriftenartikel
Publikationsstatus
Published
Erschienen in
Current Topics in Medicinal Chemistry. 2017, 17(19), pp. 2158-2165. ISSN 1568-0266. eISSN 1873-4294. Available under: doi: 10.2174/1568026617666170130121042
Zusammenfassung

Phosphoinositides (PIs) and their derivatives are essential cellular components that form the building blocks for cell membranes and regulate numerous cell functions. Specifically, the ability to generate myo-inositol 1,4,5-trisphosphate (InsP3) via phospholipase C (PLC) dependent hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) to InsP3 and diacylglycerol (DAG) initiates intracellular calcium signaling events representing a fundamental signaling mechanism dependent on PIs. InsP3 produced by PI turnover as a second messenger causes intracellular calcium release, especially from endoplasmic reticulum, by binding to the InsP3 receptor (InsP3R). Various PIs and the enzymes, such as phosphatidylinositol synthase and phosphatidylinositol 4-kinase, necessary for their turnover have been characterized in Apicomplexa, a large phylum of mostly commensal organisms that also includes several clinically relevant parasites. However, InsP3Rs have not been identified in genomes of apicomplexans, despite evidence that these parasites produce InsP3 that mediates intracellular Ca2+ signaling. Evidence to supporting IP3-dependent signaling cascades in apicomplexans suggests that they may harbor a primitive or non-canonical InsP3R. Understanding these pathways may be informative about early branching eukaryotes, where such signaling pathways also diverge from animal systems, thus identifying potential novel and essential targets for therapeutic intervention.

Zusammenfassung in einer weiteren Sprache
Fachgebiet (DDC)
570 Biowissenschaften, Biologie
Schlagwörter
Calcium signaling, InsP3 Signaling, Apicomplexan Parasites
Konferenz
Rezension
undefined / . - undefined, undefined
Zitieren
ISO 690GARCIA, Celia R.S., Eduardo ALVES, Pedro H.S. PEREIRA, Paula BARTLETT, Andrew THOMAS, Katsuhiko MIKOSHIBA, Helmut PLATTNER, L. David SIBLEY, 2017. InsP3 Signaling in Apicomplexan Parasites. In: Current Topics in Medicinal Chemistry. 2017, 17(19), pp. 2158-2165. ISSN 1568-0266. eISSN 1873-4294. Available under: doi: 10.2174/1568026617666170130121042
BibTex
@article{Garcia2017-01-30InsP3-38306,
  year={2017},
  doi={10.2174/1568026617666170130121042},
  title={InsP3 Signaling in Apicomplexan Parasites},
  number={19},
  volume={17},
  issn={1568-0266},
  journal={Current Topics in Medicinal Chemistry},
  pages={2158--2165},
  author={Garcia, Celia R.S. and Alves, Eduardo and Pereira, Pedro H.S. and Bartlett, Paula and Thomas, Andrew and Mikoshiba, Katsuhiko and Plattner, Helmut and Sibley, L. David}
}
RDF
<rdf:RDF
    xmlns:dcterms="http://purl.org/dc/terms/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
    xmlns:bibo="http://purl.org/ontology/bibo/"
    xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#"
    xmlns:foaf="http://xmlns.com/foaf/0.1/"
    xmlns:void="http://rdfs.org/ns/void#"
    xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > 
  <rdf:Description rdf:about="https://kops.uni-konstanz.de/server/rdf/resource/123456789/38306">
    <dc:language>eng</dc:language>
    <dc:creator>Alves, Eduardo</dc:creator>
    <dc:creator>Pereira, Pedro H.S.</dc:creator>
    <dc:contributor>Mikoshiba, Katsuhiko</dc:contributor>
    <dcterms:title>InsP3 Signaling in Apicomplexan Parasites</dcterms:title>
    <dc:contributor>Bartlett, Paula</dc:contributor>
    <dc:contributor>Pereira, Pedro H.S.</dc:contributor>
    <dcterms:issued>2017-01-30</dcterms:issued>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dc:creator>Plattner, Helmut</dc:creator>
    <dc:creator>Bartlett, Paula</dc:creator>
    <dcterms:abstract xml:lang="eng">Phosphoinositides (PIs) and their derivatives are essential cellular components that form the building blocks for cell membranes and regulate numerous cell functions. Specifically, the ability to generate myo-inositol 1,4,5-trisphosphate (InsP3) via phospholipase C (PLC) dependent hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) to InsP3 and diacylglycerol (DAG) initiates intracellular calcium signaling events representing a fundamental signaling mechanism dependent on PIs. InsP3 produced by PI turnover as a second messenger causes intracellular calcium release, especially from endoplasmic reticulum, by binding to the InsP3 receptor (InsP3R). Various PIs and the enzymes, such as phosphatidylinositol synthase and phosphatidylinositol 4-kinase, necessary for their turnover have been characterized in Apicomplexa, a large phylum of mostly commensal organisms that also includes several clinically relevant parasites. However, InsP3Rs have not been identified in genomes of apicomplexans, despite evidence that these parasites produce InsP3 that mediates intracellular Ca2+ signaling. Evidence to supporting IP3-dependent signaling cascades in apicomplexans suggests that they may harbor a primitive or non-canonical InsP3R. Understanding these pathways may be informative about early branching eukaryotes, where such signaling pathways also diverge from animal systems, thus identifying potential novel and essential targets for therapeutic intervention.</dcterms:abstract>
    <dc:contributor>Alves, Eduardo</dc:contributor>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dc:contributor>Thomas, Andrew</dc:contributor>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2017-04-04T12:35:49Z</dc:date>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2017-04-04T12:35:49Z</dcterms:available>
    <dc:contributor>Plattner, Helmut</dc:contributor>
    <dc:creator>Mikoshiba, Katsuhiko</dc:creator>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <bibo:uri rdf:resource="https://kops.uni-konstanz.de/handle/123456789/38306"/>
    <dc:contributor>Sibley, L. David</dc:contributor>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:contributor>Garcia, Celia R.S.</dc:contributor>
    <dc:creator>Thomas, Andrew</dc:creator>
    <dc:creator>Sibley, L. David</dc:creator>
    <dc:creator>Garcia, Celia R.S.</dc:creator>
  </rdf:Description>
</rdf:RDF>
Interner Vermerk
xmlui.Submission.submit.DescribeStep.inputForms.label.kops_note_fromSubmitter
Kontakt
URL der Originalveröffentl.
Prüfdatum der URL
Prüfungsdatum der Dissertation
Finanzierungsart
Kommentar zur Publikation
Allianzlizenz
Corresponding Authors der Uni Konstanz vorhanden
Internationale Co-Autor:innen
Universitätsbibliographie
Begutachtet