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rdf:type |
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lifeskim:mentions |
umls-concept:C0017337,
umls-concept:C0085862,
umls-concept:C0441712,
umls-concept:C0596290,
umls-concept:C0597298,
umls-concept:C0752312,
umls-concept:C1299583,
umls-concept:C1366765,
umls-concept:C1424650,
umls-concept:C1523987,
umls-concept:C1539079,
umls-concept:C1549571,
umls-concept:C1608386
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pubmed:issue |
1
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pubmed:dateCreated |
2006-12-15
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pubmed:abstractText |
sef (similar expression to fgf genes) was recently identified as a negative regulator of fibroblast growth factor (FGF) signaling in zebrafish, chicken, mouse and human. By repressing events upstream and/or downstream Ras, Sef inhibits FGF-induced ERK activation and cell proliferation. Here we report that Sef-S, an alternative splice isoform of Sef, lacks a signal peptide and is localized in cytosol. Sef-S inhibits FGF-induced NIH3T3 cell proliferation, a similar function to Sef. However, Sef-S represses neither the intensity nor the duration of ERK activation. Moreover, Sef-S does not inhibit Elk1-dependent transcription. Our study revealed that the signal peptide is critical for the different activities between Sef and Sef-S in FGF-Ras-MAPK signaling cascades. Furthermore, we observed that Sef-S associated with FGFR2 in a co-immunoprecipitated complex. These results indicate that Sef-S inhibits FGF-induced NIH3T3 cell proliferation via an ERK-independent mechanism and therefore suggest that alternative splice licenses sef gene to inhibit cell proliferation via multiple signaling pathways.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Elk1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Fgfr2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Fibroblast Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Isoforms,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Sorting Signals,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Fibroblast Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/Sef protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/ets-Domain Protein Elk-1
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0898-6568
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
19
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
93-102
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16857343-Alternative Splicing,
pubmed-meshheading:16857343-Amino Acid Sequence,
pubmed-meshheading:16857343-Animals,
pubmed-meshheading:16857343-Base Sequence,
pubmed-meshheading:16857343-Cell Proliferation,
pubmed-meshheading:16857343-Cytosol,
pubmed-meshheading:16857343-Enzyme Activation,
pubmed-meshheading:16857343-Fibroblast Growth Factors,
pubmed-meshheading:16857343-Membrane Proteins,
pubmed-meshheading:16857343-Mice,
pubmed-meshheading:16857343-Mitogen-Activated Protein Kinase 1,
pubmed-meshheading:16857343-Mitogen-Activated Protein Kinase 3,
pubmed-meshheading:16857343-Molecular Sequence Data,
pubmed-meshheading:16857343-NIH 3T3 Cells,
pubmed-meshheading:16857343-Protein Isoforms,
pubmed-meshheading:16857343-Protein Sorting Signals,
pubmed-meshheading:16857343-Receptor, Fibroblast Growth Factor, Type 2,
pubmed-meshheading:16857343-Signal Transduction,
pubmed-meshheading:16857343-Transcriptional Activation,
pubmed-meshheading:16857343-ets-Domain Protein Elk-1
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pubmed:year |
2007
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pubmed:articleTitle |
Sef-S, an alternative splice isoform of sef gene, inhibits NIH3T3 cell proliferation via a mitogen-activated protein kinases p42 and p44 (ERK1/2)-independent mechanism.
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pubmed:affiliation |
Tsinghua Institute of Genome Research, Department of Biological Sciences and Biotechnology, and School of Medicine, Tsinghua University, Beijing 100084, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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