|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
11
|
|
pubmed:dateCreated |
2005-10-21
|
|
pubmed:abstractText |
Transforming growth factor-beta-activated kinase 1 (TAK1) has been linked to interleukin 1 receptor and tumor necrosis factor receptor signaling. Here we generated mouse strains with conditional expression of a Map3k7 allele encoding part of TAK1. TAK1-deficient embryonic fibroblasts demonstrated loss of responses to interleukin 1beta and tumor necrosis factor. Studies of mice with B cell-specific TAK1 deficiency showed that TAK1 was indispensable for cellular responses to Toll-like receptor ligands, CD40 and B cell receptor crosslinking. In addition, antigen-induced immune responses were considerably impaired in mice with B cell-specific TAK1 deficiency. TAK1-deficient cells failed to activate transcription factor NF-kappaB and mitogen-activated protein kinases in response to interleukin 1beta, tumor necrosis factor and Toll-like receptor ligands. However, TAK1-deficient B cells were able to activate NF-kappaB but not the kinase Jnk in response to B cell receptor stimulation. These results collectively indicate that TAK1 is key in the cellular response to a variety of stimuli.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD40,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/MAP Kinase Kinase Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/MAP kinase kinase kinase 7,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, B-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Nov
|
|
pubmed:issn |
1529-2908
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
6
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
1087-95
|
|
pubmed:dateRevised |
2011-11-2
|
|
pubmed:meshHeading |
pubmed-meshheading:16186825-Animals,
pubmed-meshheading:16186825-Antigens, CD40,
pubmed-meshheading:16186825-B-Lymphocytes,
pubmed-meshheading:16186825-Embryo, Mammalian,
pubmed-meshheading:16186825-Fibroblasts,
pubmed-meshheading:16186825-Gene Deletion,
pubmed-meshheading:16186825-Immunity, Innate,
pubmed-meshheading:16186825-Interleukin-17,
pubmed-meshheading:16186825-Lymphopoiesis,
pubmed-meshheading:16186825-MAP Kinase Kinase Kinases,
pubmed-meshheading:16186825-Membrane Glycoproteins,
pubmed-meshheading:16186825-Mice,
pubmed-meshheading:16186825-Mice, Mutant Strains,
pubmed-meshheading:16186825-NF-kappa B,
pubmed-meshheading:16186825-Receptors, Antigen, B-Cell,
pubmed-meshheading:16186825-Receptors, Cell Surface,
pubmed-meshheading:16186825-Toll-Like Receptors,
pubmed-meshheading:16186825-Tumor Necrosis Factor-alpha
|
|
pubmed:year |
2005
|
|
pubmed:articleTitle |
Essential function for the kinase TAK1 in innate and adaptive immune responses.
|
|
pubmed:affiliation |
Akira Innate Immunity Project, Exploratory Research for Advanced Technology, Japan Science and Technology Agency.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
