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Identification of a panel of MYC and Tip60 co-regulated genes functioning primarily in cell cycle and DNA replication.
Genes Cancer
March 2018
Department of Microbiology and Molecular Immunology, Saint Louis University School of Medicine, Doisy Research Center, St. Louis, Missouri, USA.
We recently reported that adenovirus E1A enhances MYC association with the NuA4/Tip60 histone acetyltransferase (HAT) complex to activate a panel of genes enriched for DNA replication and cell cycle. Genes from this panel are highly expressed in examined cancer cell lines when compared to normal fibroblasts. To further understand gene regulation in cancer by MYC and the NuA4 complex, we performed RNA-seq analysis of MD-MB231 breast cancer cells following knockdown of MYC or Tip60 - the HAT enzyme of the NuA4 complex.
View Article and Find Full Text PDFEnhanced MYC association with the NuA4 histone acetyltransferase complex mediated by the adenovirus E1A N-terminal domain activates a subset of MYC target genes highly expressed in cancer cells.
Genes Cancer
November 2017
Department of Microbiology and Molecular Immunology/Institute for Molecular Virology, Saint Louis University School of Medicine, Doisy Research Center, St. Louis, Missouri, USA.
The proto-oncogene MYC is a transcription factor over-expressed in many cancers and required for cell survival. Its function is regulated by histone acetyltransferase (HAT) complexes, such as the GCN5 complex and the NuA4/Tip60 complex. However, the roles of the HAT complexes during MYC function in cancer have not been well characterized.
View Article and Find Full Text PDFAdenovirus E1A TRRAP-targeting domain-mediated enhancement of MYC association with the NuA4 complex activates a panel of MYC target genes enriched for gene expression and ribosome biogenesis.
Virology
December 2017
Department of Microbiology and Molecular Immunology/Institute for Molecular Virology, Saint Louis University School of Medicine, Doisy Research Center, Rm 633, 1205 Carr Lane, St. Louis, MO 63104, USA. Electronic address:
Cellular transformation by adenovirus E1A requires targeting TRRAP, a scaffold protein which helps assemble histone acetyltransferase complexes, including the NuA4 complex. We recently reported that E1A and E1A 1-80 (N-terminal 80 aa) promote association of the proto-oncogene product MYC with the NuA4 complex. The E1A N-terminal TRRAP-targeting (ET) domain is required for E1A 1-80 to interact with the NuA4 complex.
View Article and Find Full Text PDFAd E1A 243R oncoprotein promotes association of proto-oncogene product MYC with the NuA4/Tip60 complex via the E1A N-terminal repression domain.
Virology
December 2016
Department of Microbiology and Molecular Immunology/Institute for Molecular Virology, Saint Louis University School of Medicine, Doisy Research Center, St. Louis, MO 63104, USA. Electronic address:
The adenovirus E1A 243R oncoprotein targets TRRAP, a scaffold protein that assembles histone acetyltransferase (HAT) complexes, such as the NuA4/Tip60 complex which mediates transcriptional activity of the proto-oncogene MYC and helps determine the cancer cell phenotype. How E1A transforms cells through TRRAP remains obscure. We performed proteomic analysis with the N-terminal transcriptional repression domain of E1A 243R (E1A 1-80) and showed that E1A 1-80 interacts with TRRAP, p400, and three other members of the NuA4 complex - DMAP1, RUVBL1 and RUVBL2 - not previously shown to associate with E1A 243R.
View Article and Find Full Text PDFThe adenoviral E1A N-terminal domain represses MYC transcription in human cancer cells by targeting both p300 and TRRAP and inhibiting MYC promoter acetylation of H3K18 and H4K16.
Genes Cancer
March 2016
Institute for Molecular Virology, Department of Microbiology and Molecular Immunology, Saint Louis University School of Medicine, Doisy Research Center, St. Louis, Missouri, USA.
Human cancers frequently arise from increased expression of proto-oncogenes, such as MYC and HER2. Understanding the cellular pathways regulating the transcription and expression of proto-oncogenes is important for targeted therapies for cancer treatment. Adenoviral (Ad) E1A 243R (243 aa residues) is a viral oncoprotein that interacts with key regulators of gene transcription and cell proliferation.
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