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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0017262,
umls-concept:C0021665,
umls-concept:C0037663,
umls-concept:C0086418,
umls-concept:C0122592,
umls-concept:C0127400,
umls-concept:C0205147,
umls-concept:C1519726,
umls-concept:C1704259,
umls-concept:C1705987,
umls-concept:C1707271,
umls-concept:C1948023
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pubmed:issue |
1
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pubmed:dateCreated |
2003-12-18
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pubmed:abstractText |
The signaling pathway of GH-stimulated IGF-I gene expression is still unclear, although it has been reported that the Janus kinase (JAK)-signal transducers and activators of transcription (STAT)5b pathway plays an important role in liver IGF-I expression. In this study, the GH-dependent IGF-I gene expression and its intracellular signaling mechanism have been examined in mouse pro-B, Ba/F3 cells stably expressing human GH receptor (Ba/F3-hGHR). The IGF-I gene expression was stimulated by human GH (0.01-10 nm) in a dose-dependent fashion in Ba/F3-hGHR cells. The specific inhibitors for JAK2 remarkably suppressed the GH-induced IGF-I gene expression, but MAPK or phosphatidylinositol 3 kinase-specific inhibitors failed to block the GH stimulation of the IGF-I gene expression. However, genistein, a nonspecific tyrosine kinase inhibitor that does not inhibit JAK2 and STAT5 phosphorylation, significantly suppressed the GH-induced IGF-I gene expression. Additionally, a Ba/F3-hGHR mutant that contained the truncated C-terminal hGHR up to D351 showed no IGF-I gene expression in response to human GH. The D351 form normally has the GH-induced JAK/STAT5 tyrosine phosphorylation. These results suggest that the JAK-STAT5 pathway and the novel tyrosine phosphorylation pathway, dependent on signaling from the C-terminal region of hGHR, might be involved in the GH-stimulated IGF-I gene expression in Ba/F3 cells.
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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/Cycloheximide,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/JAK2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Jak2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Janus Kinase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Milk Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Synthesis Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Somatotropin,
http://linkedlifedata.com/resource/pubmed/chemical/STAT5 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0013-7227
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
145
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
214-20
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:14551225-Animals,
pubmed-meshheading:14551225-Cells, Cultured,
pubmed-meshheading:14551225-Cycloheximide,
pubmed-meshheading:14551225-DNA-Binding Proteins,
pubmed-meshheading:14551225-Gene Expression,
pubmed-meshheading:14551225-Growth Hormone,
pubmed-meshheading:14551225-Humans,
pubmed-meshheading:14551225-Insulin-Like Growth Factor I,
pubmed-meshheading:14551225-Janus Kinase 2,
pubmed-meshheading:14551225-Mice,
pubmed-meshheading:14551225-Milk Proteins,
pubmed-meshheading:14551225-Mitogen-Activated Protein Kinases,
pubmed-meshheading:14551225-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:14551225-Phosphorylation,
pubmed-meshheading:14551225-Protein Structure, Tertiary,
pubmed-meshheading:14551225-Protein Synthesis Inhibitors,
pubmed-meshheading:14551225-Protein-Tyrosine Kinases,
pubmed-meshheading:14551225-Proto-Oncogene Proteins,
pubmed-meshheading:14551225-RNA, Messenger,
pubmed-meshheading:14551225-Receptors, Somatotropin,
pubmed-meshheading:14551225-STAT5 Transcription Factor,
pubmed-meshheading:14551225-Signal Transduction,
pubmed-meshheading:14551225-Trans-Activators,
pubmed-meshheading:14551225-Tyrosine
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pubmed:year |
2004
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pubmed:articleTitle |
Growth hormone (GH)-stimulated insulin-like growth factor I gene expression is mediated by a tyrosine phosphorylation pathway depending on C-terminal region of human GH receptor in human GH receptor-expressing Ba/F3 cells.
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pubmed:affiliation |
Department of Materials Science and Engineering, Nagoya Institute of Technology, Nagoya 466-8555, Japan. h-yoshi@ks.kyy.nitech.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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