rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
1989-7-31
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pubmed:abstractText |
We have observed that a 2-h pretreatment of murine B cells with cholera toxin (CT) renders the B cell incapable of receiving an activation signal via surface Ig as measured by cell volume increase and entry into the S phase of the cell cycle. In contrast, CT pretreatment does not inhibit the delivery of a signal by IL-4, as measured by increase in cell volume. In fact, CT pretreated B cells are able to respond to anti-Ig in the presence of IL-4, as measured by both an increase in cell size and entry into S suggesting that IL-4 overcomes the effects of CT on normal B cell activation. Despite blocking the anti-Ig-mediated entry into the cell cycle, CT was not able to interfere with the induction of nonresponsiveness by anti-Ig in normal B cells or with the delivery of growth-inhibitory signal to the B cell lymphoma WEHI-231. These results suggest that there are two signaling pathways mediated by cross-linking of surface Ig: one pathway sensitive and the other insensitive to modulation by CT.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Anti-Idiotypic,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cholera Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol Phosphates,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, B-Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
143
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
458-63
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2786908-Animals,
pubmed-meshheading:2786908-Antibodies, Anti-Idiotypic,
pubmed-meshheading:2786908-B-Lymphocytes,
pubmed-meshheading:2786908-Calcium,
pubmed-meshheading:2786908-Cell Line,
pubmed-meshheading:2786908-Cholera Toxin,
pubmed-meshheading:2786908-Histocompatibility Antigens Class II,
pubmed-meshheading:2786908-Inositol Phosphates,
pubmed-meshheading:2786908-Interleukin-4,
pubmed-meshheading:2786908-Interleukins,
pubmed-meshheading:2786908-Kinetics,
pubmed-meshheading:2786908-Lipopolysaccharides,
pubmed-meshheading:2786908-Lymphocyte Activation,
pubmed-meshheading:2786908-Lymphoma,
pubmed-meshheading:2786908-Mice,
pubmed-meshheading:2786908-Receptors, Antigen, B-Cell,
pubmed-meshheading:2786908-Signal Transduction
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pubmed:year |
1989
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pubmed:articleTitle |
Cholera toxin-sensitive and insensitive signaling via surface Ig.
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pubmed:affiliation |
Immunology Unit, University of Rochester Cancer Center, NY 14642.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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