Redox regulation of CD21 shedding involves signaling via PKC and indicates the formation of a juxtamembrane stalk

Aichem, Annette; Masilamani, Madhan; Illges, Harald

Redox regulation of CD21 shedding involves signaling via PKC and indicates the formation of a juxtamembrane stalk

Dateien

Zu diesem Dokument gibt es keine Dateien.

Datum

2006

Autor:innen

Aichem, Annette

Masilamani, Madhan

Illges, Harald

DOI (zitierfähiger Link)

https://doi.org/10.1242/jcs.02984

Sammlungen

Biologie

Publikationstyp

Zeitschriftenartikel

Publikationsstatus

Published

Erschienen in

Journal of Cell Science. Company of Biologists. 2006, 119(14), pp. 2892-2902. ISSN 0021-9533. eISSN 1477-9137. Available under: doi: 10.1242/jcs.02984

Zusammenfassung

Soluble CD21 (sCD21), released from the plasma membrane by proteolytic cleavage (shedding) of its extracellular domain (ectodomain) blocks B cell/follicular dendritic cell interaction and activates monocytes. We show here that both serine- and metalloproteases are involved in CD21 shedding. Using the oxidant pervanadate to mimic B cell receptor activation and thiol antioxidants such as N-acetylcysteine (NAC) and glutathione (GSH) we show that CD21 shedding is a redox-regulated process inducible by oxidation presumably through activation of a tyrosine kinase-mediated signal pathway involving protein kinase C (PKC), and by reducing agents that either directly activate the metalloprotease and/or modify intramolecular disulfide bridges within CD21 and thereby facilitate access to the cleavage site. Lack of short consensus repeat 16 (SCR16) abolishes CD21 shedding, and opening of the disulfide bridge between cys-2 (Cys941) and cys-4 (Cys968) of SCR16 is a prerequisite for CD21 shedding. Replacing these cysteines with selenocysteines (thereby changing the redox potential from -180 to -381 mV) results in a loss of inducible CD21 shedding, and removing this bridge by exchanging these cysteines with methionines increases CD21 shedding.

Fachgebiet (DDC)

570 Biowissenschaften, Biologie

Schlagwörter

B cells, CD21, Complement receptor, Cell activation, Redox potential, Selenocysteine, Diselenide bridge

Zitieren

ISO 690

AICHEM, Annette, Madhan MASILAMANI, Harald ILLGES, 2006. Redox regulation of CD21 shedding involves signaling via PKC and indicates the formation of a juxtamembrane stalk. In: Journal of Cell Science. Company of Biologists. 2006, 119(14), pp. 2892-2902. ISSN 0021-9533. eISSN 1477-9137. Available under: doi: 10.1242/jcs.02984

BibTex

@article{Aichem2006-07-15Redox-49728,
  year={2006},
  doi={10.1242/jcs.02984},
  title={Redox regulation of CD21 shedding involves signaling via PKC and indicates the formation of a juxtamembrane stalk},
  number={14},
  volume={119},
  issn={0021-9533},
  journal={Journal of Cell Science},
  pages={2892--2902},
  author={Aichem, Annette and Masilamani, Madhan and Illges, Harald}
}

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/123456789/49728">
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:creator>Aichem, Annette</dc:creator>
    <dc:contributor>Aichem, Annette</dc:contributor>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dcterms:title>Redox regulation of CD21 shedding involves signaling via PKC and indicates the formation of a juxtamembrane stalk</dcterms:title>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-05-28T12:18:39Z</dcterms:available>
    <dc:contributor>Illges, Harald</dc:contributor>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dc:rights>terms-of-use</dc:rights>
    <dc:creator>Illges, Harald</dc:creator>
    <dcterms:abstract xml:lang="eng">Soluble CD21 (sCD21), released from the plasma membrane by proteolytic cleavage (shedding) of its extracellular domain (ectodomain) blocks B cell/follicular dendritic cell interaction and activates monocytes. We show here that both serine- and metalloproteases are involved in CD21 shedding. Using the oxidant pervanadate to mimic B cell receptor activation and thiol antioxidants such as N-acetylcysteine (NAC) and glutathione (GSH) we show that CD21 shedding is a redox-regulated process inducible by oxidation presumably through activation of a tyrosine kinase-mediated signal pathway involving protein kinase C (PKC), and by reducing agents that either directly activate the metalloprotease and/or modify intramolecular disulfide bridges within CD21 and thereby facilitate access to the cleavage site. Lack of short consensus repeat 16 (SCR16) abolishes CD21 shedding, and opening of the disulfide bridge between cys-2 (Cys941) and cys-4 (Cys968) of SCR16 is a prerequisite for CD21 shedding. Replacing these cysteines with selenocysteines (thereby changing the redox potential from -180 to -381 mV) results in a loss of inducible CD21 shedding, and removing this bridge by exchanging these cysteines with methionines increases CD21 shedding.</dcterms:abstract>
    <dc:contributor>Masilamani, Madhan</dc:contributor>
    <dcterms:issued>2006-07-15</dcterms:issued>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/>
    <dc:language>eng</dc:language>
    <dc:creator>Masilamani, Madhan</dc:creator>
    <bibo:uri rdf:resource="https://kops.uni-konstanz.de/handle/123456789/49728"/>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-05-28T12:18:39Z</dc:date>
  </rdf:Description>
</rdf:RDF>

Begutachtet

Ja