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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2000-1-4
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pubmed:abstractText |
To study the function of Ig-alpha in the selection of autoreactive B cells, we have analyzed mb-1 cytoplasmic truncation mutant mice (mb-1delta(c)/delta(c)), which coexpress transgenes encoding hen egg lysozyme (HEL) and HEL-specific immunoglobulin. We demonstrate that in the presence of soluble HEL (sHEL) and dependent on the mb-1delta(c) mutation, most immature B cells bearing the HEL-specific Ig transgene undergo rearrangements of endogenous kappa light chains, resulting in loss of HEL specificity. Moreover, immature B cells from Ig-alpha mutant mice respond to BCR cross-linking with an exaggerated and prolonged calcium response and induction of protein tyrosine phosphorylation. Our data imply a negative signaling role for Ig-alpha in immature B cells.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD79,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Cd79a protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin kappa-Chains,
http://linkedlifedata.com/resource/pubmed/chemical/Muramidase,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, B-Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1074-7613
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
11
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
537-45
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:10591179-Animals,
pubmed-meshheading:10591179-Antibody Specificity,
pubmed-meshheading:10591179-Antigens, CD,
pubmed-meshheading:10591179-Antigens, CD79,
pubmed-meshheading:10591179-Apoptosis,
pubmed-meshheading:10591179-Autoantigens,
pubmed-meshheading:10591179-Calcium Signaling,
pubmed-meshheading:10591179-Clonal Deletion,
pubmed-meshheading:10591179-Crosses, Genetic,
pubmed-meshheading:10591179-Gene Rearrangement, B-Lymphocyte, Light Chain,
pubmed-meshheading:10591179-Immunoglobulin kappa-Chains,
pubmed-meshheading:10591179-Immunologic Capping,
pubmed-meshheading:10591179-Lymphocyte Activation,
pubmed-meshheading:10591179-Mice,
pubmed-meshheading:10591179-Mice, Inbred C57BL,
pubmed-meshheading:10591179-Mice, Transgenic,
pubmed-meshheading:10591179-Muramidase,
pubmed-meshheading:10591179-Mutagenesis, Site-Directed,
pubmed-meshheading:10591179-Phosphorylation,
pubmed-meshheading:10591179-Protein Processing, Post-Translational,
pubmed-meshheading:10591179-Protein Structure, Tertiary,
pubmed-meshheading:10591179-Protein-Tyrosine Kinases,
pubmed-meshheading:10591179-Receptors, Antigen, B-Cell,
pubmed-meshheading:10591179-Sequence Deletion,
pubmed-meshheading:10591179-Terminator Regions, Genetic
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pubmed:year |
1999
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pubmed:articleTitle |
Ig-alpha cytoplasmic truncation renders immature B cells more sensitive to antigen contact.
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pubmed:affiliation |
Department of Immunology, Institute for Genetics, University of Cologne, Germany. m.kraus@uni-koeln.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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