rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
12
|
pubmed:dateCreated |
1998-7-9
|
pubmed:abstractText |
SEK1 (MKK4/JNKK) is a mitogen-activated protein kinase activator that has been shown to participate in vitro in two stress-activated cascades terminating with the SAPK and p38 kinases. To define the role of SEK1 in vivo, we studied stress-induced signaling in SEK1(-/-) embryonic stem and fibroblast cells and evaluated the phenotype of SEK1(-/-) mouse embryos during development. Studies of SEK1(-/-) embryonic stem cells demonstrated defects in stimulated SAPK phosphorylation but not in the phosphorylation of p38 kinase. In contrast, SEK1(-/-) fibroblasts exhibited defects in both SAPK and p38 phosphorylation, demonstrating that crosstalk exists between the stress-activated cascades. Tumor necrosis factor alpha and interleukin 1 stimulation of both stress-activated cascades are severely affected in the SEK1(-/-) fibroblast cells. SEK1 deficiency leads to embryonic lethality after embryonic day 12.5 and is associated with abnormal liver development. This phenotype is similar to c-jun null mouse embryos and suggests that SEK1 is required for phosphorylation and activation of c-jun during the organo-genesis of the liver.
|
pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-1569957,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-1692099,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-2744271,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-7513319,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-7603567,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-7834738,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-7839144,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-7854452,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-7854453,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-7860764,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-7997269,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-7997270,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8137421,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8177321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8254036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8330736,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8371760,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8557196,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8565820,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8702807,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8791420,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8793994,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8877106,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8917510,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8917518,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-8918464,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-9002521,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-9013568,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-9069290,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-9096336,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-9129010,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-9148940,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-9184210,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-9199291,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9618507-9207092
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
0027-8424
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
9
|
pubmed:volume |
95
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
6881-6
|
pubmed:dateRevised |
2009-11-19
|
pubmed:meshHeading |
pubmed-meshheading:9618507-Animals,
pubmed-meshheading:9618507-Calcium-Calmodulin-Dependent Protein Kinases,
pubmed-meshheading:9618507-Fibroblasts,
pubmed-meshheading:9618507-Gene Expression Regulation, Developmental,
pubmed-meshheading:9618507-Liver,
pubmed-meshheading:9618507-MAP Kinase Kinase 4,
pubmed-meshheading:9618507-Mice,
pubmed-meshheading:9618507-Mice, Knockout,
pubmed-meshheading:9618507-Mitogen-Activated Protein Kinase Kinases,
pubmed-meshheading:9618507-Protein Kinases,
pubmed-meshheading:9618507-Signal Transduction,
pubmed-meshheading:9618507-Stem Cells
|
pubmed:year |
1998
|
pubmed:articleTitle |
SEK1 deficiency reveals mitogen-activated protein kinase cascade crossregulation and leads to abnormal hepatogenesis.
|
pubmed:affiliation |
Division of Hematology/Oncology, Children's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|