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rdf:type |
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lifeskim:mentions |
umls-concept:C0004561,
umls-concept:C0152060,
umls-concept:C0205154,
umls-concept:C0205263,
umls-concept:C0301625,
umls-concept:C0851285,
umls-concept:C1306235,
umls-concept:C1421249,
umls-concept:C1514873,
umls-concept:C1518440,
umls-concept:C1522492,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636
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pubmed:issue |
9
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pubmed:dateCreated |
2002-10-22
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pubmed:abstractText |
IFN-alpha inhibits B lymphocyte development, and the nuclear protein Daxx has been reported to be essential for this biological activity. We show in this study that IFN-alpha inhibits the clonal proliferation of B lymphocyte progenitors in response to IL-7 in wild-type, but not in tyk2-deficient, mice. In addition, the IFN-alpha-induced up-regulation and nuclear translocation of Daxx are completely abrogated in the absence of tyk2. Therefore, tyk2 is directly involved in IFN-alpha signaling for the induction and translocation of Daxx, which may result in B lymphocyte growth arrest and/or apoptosis.
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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/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Daxx protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-7,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/TYK2 Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Tyk2 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-1767
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pubmed:author |
pubmed-author:AokiKenichiK,
pubmed-author:GondoHisashiH,
pubmed-author:HaradaMineM,
pubmed-author:ImamuraRieR,
pubmed-author:KamesakiKenjirouK,
pubmed-author:KatoKoujiK,
pubmed-author:MatsudaTadashiT,
pubmed-author:MiyamotoToshihiroT,
pubmed-author:NagafuchiSeihoS,
pubmed-author:NagafujiKojiK,
pubmed-author:NakayamaKei-IchiK,
pubmed-author:NumataAkihikoA,
pubmed-author:OritaniKenjiK,
pubmed-author:ShimodaKazuyaK,
pubmed-author:TakaseKenK,
pubmed-author:TamiyaSadafumiS,
pubmed-author:YamamotoTetsuyaT
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
169
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4707-11
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12391177-Active Transport, Cell Nucleus,
pubmed-meshheading:12391177-Animals,
pubmed-meshheading:12391177-B-Lymphocytes,
pubmed-meshheading:12391177-Bone Marrow Cells,
pubmed-meshheading:12391177-Carrier Proteins,
pubmed-meshheading:12391177-Cell Differentiation,
pubmed-meshheading:12391177-Cell Line,
pubmed-meshheading:12391177-Cells, Cultured,
pubmed-meshheading:12391177-Coculture Techniques,
pubmed-meshheading:12391177-Growth Inhibitors,
pubmed-meshheading:12391177-Hematopoietic Stem Cells,
pubmed-meshheading:12391177-Immunosuppressive Agents,
pubmed-meshheading:12391177-Interferon-alpha,
pubmed-meshheading:12391177-Interleukin-7,
pubmed-meshheading:12391177-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:12391177-Mice,
pubmed-meshheading:12391177-Mice, Knockout,
pubmed-meshheading:12391177-Nuclear Proteins,
pubmed-meshheading:12391177-Protein-Tyrosine Kinases,
pubmed-meshheading:12391177-Proteins,
pubmed-meshheading:12391177-TYK2 Kinase
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pubmed:year |
2002
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pubmed:articleTitle |
Cutting edge: tyk2 is required for the induction and nuclear translocation of Daxx which regulates IFN-alpha-induced suppression of B lymphocyte formation.
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pubmed:affiliation |
First Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan. kshimoda@intmed1.med.kyushu-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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