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rdf:type |
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lifeskim:mentions |
umls-concept:C0004561,
umls-concept:C0017262,
umls-concept:C0038952,
umls-concept:C0044602,
umls-concept:C0242606,
umls-concept:C0285761,
umls-concept:C0332157,
umls-concept:C0851285,
umls-concept:C1150481,
umls-concept:C1368105,
umls-concept:C1415020,
umls-concept:C1451005,
umls-concept:C1704259,
umls-concept:C1705325,
umls-concept:C1705987,
umls-concept:C1879547,
umls-concept:C2587213
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pubmed:issue |
4
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pubmed:dateCreated |
2011-2-28
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pubmed:abstractText |
Histone acetyltransferase(s) (HATs) are involved in the acetylation of core histones, which is an important event for transcription regulation through alterations in the chromatin structure in eukaryotes. General control non-depressible 5 (GCN5) was first identified as a global coactivator and transcription-related HAT. Here we report that GCN5 regulates the activation of phosphatidylinositol 3-kinase (PI3K)/acutely transforming retrovirus AKT8 in rodent T cell lymphoma (Akt) survival pathway in B cells exposed to oxidative stress via controlling gene expressions of spleen tyrosine kinase (Syk) and Bruton's tyrosine kinase (Btk). The GCN5-deficiency remarkably caused apoptotic cell death by treatment with exogenous hydrogen peroxide (H(2)O(2)) in chicken DT40 cells. In GCN5-deficient DT40 cells, gene expressions of Syk and Btk, which are involved in activation of PI3K/Akt survival pathway in DT40 cells exposed to exogenous H(2)O(2), were remarkably decreased compared with those in wild type DT40 cells. In addition, phosphorylation of Akt in H(2)O(2)-treated GCN5-deficient cells was remarkably suppressed as compared to that of DT40. Chromatin immunoprecipitation assay revealed that GCN5 binds to proximal 5'-upstream regions of Syk and Btk genes in vivo. These results suggest that GCN5 takes part in transcriptional regulations of the Syk and Btk genes, and plays a key role in epigenetic regulation of PI3K/Akt survival pathway in B cells exposed to reactive oxygen species such as H(2)O(2).
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1090-2104
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pubmed:author |
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pubmed:copyrightInfo |
Copyright © 2011 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
25
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pubmed:volume |
405
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
657-61
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pubmed:dateRevised |
2011-11-2
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pubmed:meshHeading |
pubmed-meshheading:21281601-Animals,
pubmed-meshheading:21281601-Apoptosis,
pubmed-meshheading:21281601-B-Lymphocytes,
pubmed-meshheading:21281601-Cell Line,
pubmed-meshheading:21281601-Chickens,
pubmed-meshheading:21281601-Chromatin Immunoprecipitation,
pubmed-meshheading:21281601-Enzyme Activation,
pubmed-meshheading:21281601-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:21281601-Hydrogen Peroxide,
pubmed-meshheading:21281601-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:21281601-Mutation,
pubmed-meshheading:21281601-Oxidative Stress,
pubmed-meshheading:21281601-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:21281601-Protein-Tyrosine Kinases,
pubmed-meshheading:21281601-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:21281601-p300-CBP Transcription Factors
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pubmed:year |
2011
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pubmed:articleTitle |
GCN5 regulates the activation of PI3K/Akt survival pathway in B cells exposed to oxidative stress via controlling gene expressions of Syk and Btk.
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pubmed:affiliation |
Section of Biochemistry and Molecular Biology, Department of Medical Sciences, Miyazaki Medical College, University of Miyazaki, Kiyotake, Miyazaki 889-1692, Japan. masakari@med.miyazaki-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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