Document Detail

KyoT3, an isoform of murine FHL1, associates with the transcription factor RBP-J and represses the RBP-J-mediated transactivation.
MedLine Citation:
PMID:  18760388     Owner:  NLM     Status:  MEDLINE    
Previously, we have shown that KyoT2, an isoform of the four and a half LIM domain protein 1 (FHL1), modulates Notch signaling via repressing RBP-J-mediated transactivation. In this study, we investigated the effect of another isoform of FHL1, KyoT3, on transactivation of a RBP-J-dependent promoter. We found that KyoT3 was expressed widely in a variety of tissues. By constructing EGFP fusion proteins, we showed that KyoT3 locates preferentially in nucleus. KyoT3 interacted with RBP-J, as shown by co-immunoprecipitation assays. Moreover, we demonstrated by a reporter assay that KyoT3 repressed transactivation of a RBP-J-dependent promoter, which was activated by both the Notch intracellular domain and Epstein-Barr virus nuclear antigen 2, an EB virus-encoded oncoprotein. These results suggest a multi-elemental control of the Notch signaling pathway, which is critical for cell differentiation in development.
Liang Liang; Hong-Wei Zhang; Jie Liang; Xiao-Li Niu; Su-Zhen Zhang; Lei Feng; Ying-Min Liang; Hua Han
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-08-09
Journal Detail:
Title:  Biochimica et biophysica acta     Volume:  1779     ISSN:  0006-3002     ISO Abbreviation:  Biochim. Biophys. Acta     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-11-21     Completed Date:  2009-02-09     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0217513     Medline TA:  Biochim Biophys Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  805-10     Citation Subset:  IM    
State Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Fourth Military Medical University, Xi'an 710032, PR China.
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MeSH Terms
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / genetics,  physiology*
Cell Differentiation
Cell Nucleus / metabolism
Epstein-Barr Virus Nuclear Antigens / metabolism
Gene Expression Regulation*
Genes, Reporter
Hela Cells
Immunoglobulin J Recombination Signal Sequence-Binding Protein
Models, Biological
Muscle Proteins / metabolism,  physiology*
Promoter Regions, Genetic
Protein Binding
Transcriptional Activation*
Viral Proteins / metabolism
Reg. No./Substance:
0/Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0/EBNA-2 protein, Human herpesvirus 4; 0/Epstein-Barr Virus Nuclear Antigens; 0/Fhl1 protein, mouse; 0/Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0/Muscle Proteins; 0/Rbpj protein, mouse; 0/Viral Proteins

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