Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / genetics
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Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / physiology*
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Cell Differentiation
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Cell Nucleus / metabolism
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Epstein-Barr Virus Nuclear Antigens / metabolism
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Gene Expression Regulation*
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Genes, Reporter
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HeLa Cells
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Humans
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Immunoglobulin J Recombination Signal Sequence-Binding Protein
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Intracellular Signaling Peptides and Proteins
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LIM Domain Proteins
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Mice
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Models, Biological
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Muscle Proteins / metabolism
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Muscle Proteins / physiology*
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Promoter Regions, Genetic
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Protein Binding
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Transcriptional Activation*
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Viral Proteins / metabolism
Substances
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Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
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EBNA-2 protein, Human herpesvirus 4
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Epstein-Barr Virus Nuclear Antigens
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Fhl1 protein, mouse
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Immunoglobulin J Recombination Signal Sequence-Binding Protein
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Intracellular Signaling Peptides and Proteins
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LIM Domain Proteins
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Muscle Proteins
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Rbpj protein, mouse
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Viral Proteins