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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2007-8-6
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pubmed:abstractText |
EoL-1 cells have a FIP1L1-PDGFRA fusion gene which causes the transformation of eosinophilic precursor cells into leukemia cells. Recently, we suggested that the induction of differentiation of EoL-1 cells into eosinophils by the HDAC inhibitors apicidin and n-butyrate is due to the continuous inhibition of HDACs. However, neither apicidin nor n-butyrate inhibited the expression of FIP1L1-PDGFRA mRNA, although both these inhibitors suppressed cell proliferation. Therefore, in this study, we analyzed whether the levels of FIP1L1-PDGFRalpha protein and phosphorylated-Stat5 involved in the signaling for the proliferation of EoL-1 cells are attenuated by HDAC inhibitors.
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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/Butyrates,
http://linkedlifedata.com/resource/pubmed/chemical/FIP1L1-PDGFRA fusion protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxamic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Proteins, Fusion,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides, Cyclic,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Platelet-Derived Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/STAT5 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/apicidin,
http://linkedlifedata.com/resource/pubmed/chemical/mRNA Cleavage and Polyadenylation...,
http://linkedlifedata.com/resource/pubmed/chemical/trichostatin A
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pubmed:status |
MEDLINE
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pubmed:issn |
1423-0097
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
143 Suppl 1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
28-32
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17541273-Butyrates,
pubmed-meshheading:17541273-Cell Differentiation,
pubmed-meshheading:17541273-Cell Line, Tumor,
pubmed-meshheading:17541273-Eosinophils,
pubmed-meshheading:17541273-Gene Expression Regulation, Leukemic,
pubmed-meshheading:17541273-Histone Deacetylase Inhibitors,
pubmed-meshheading:17541273-Humans,
pubmed-meshheading:17541273-Hydroxamic Acids,
pubmed-meshheading:17541273-Hypereosinophilic Syndrome,
pubmed-meshheading:17541273-Neoplasm Proteins,
pubmed-meshheading:17541273-Oncogene Proteins, Fusion,
pubmed-meshheading:17541273-Peptides, Cyclic,
pubmed-meshheading:17541273-Phosphorylation,
pubmed-meshheading:17541273-Protein Processing, Post-Translational,
pubmed-meshheading:17541273-RNA, Messenger,
pubmed-meshheading:17541273-Receptor, Platelet-Derived Growth Factor alpha,
pubmed-meshheading:17541273-STAT5 Transcription Factor,
pubmed-meshheading:17541273-mRNA Cleavage and Polyadenylation Factors
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pubmed:year |
2007
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pubmed:articleTitle |
Mechanism for the differentiation of EoL-1 cells into eosinophils by histone deacetylase inhibitors.
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pubmed:affiliation |
Laboratory of Pathophysiological Biochemistry, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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