Author
Donald E. Ayer
Other affiliations: University of Utah, Fred Hutchinson Cancer Research Center, University of Colorado Boulder ...read more
Bio: Donald E. Ayer is an academic researcher from Huntsman Cancer Institute. The author has contributed to research in topics: Transcription factor & TXNIP. The author has an hindex of 47, co-authored 73 publications receiving 11603 citations. Previous affiliations of Donald E. Ayer include University of Utah & Fred Hutchinson Cancer Research Center.
Topics: Transcription factor, TXNIP, MLX, Corepressor, Repressor
Papers published on a yearly basis
Papers
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TL;DR: In this paper, the Max polypeptide when associated with the Myc or Mad polyPEptide is capable of binding to nucleotide sequences containing CACGTG.
Abstract: Nucleic acid molecules capable of hybridizing under stringent conditions to the nucleotide sequence residing between positions 1 and 453 of the max cDNAs shown in Figure 2, or to the nucleotide sequence reisiding between positions 148 and 810 of the mad cDNAs shown in Figure 14. The Max polypeptide when associated with the Myc or Mad polypeptide is capable of binding to nucleotide sequences containing CACGTG.
1,602 citations
TL;DR: A convergence of repression pathways for bHLH-Zip proteins and nuclear receptors is established and suggests this type of regulation may be more widely conserved than previously suspected.
1,303 citations
TL;DR: A novel class of methylated H3K4 effector domains—the PHD domains of the ING (for inhibitor of growth) family of tumour suppressor proteins—are identified and established a pivotal role for trimethylation of H 3K4 in gene repression and, potentially, tumour suppressing mechanisms.
Abstract: Dynamic regulation of diverse nuclear processes is intimately linked to covalent modifications of chromatin. Much attention has focused on methylation at lysine 4 of histone H3 (H3K4), owing to its association with euchromatic genomic regions. H3K4 can be mono-, di- or tri-methylated. Trimethylated H3K4 (H3K4me3) is preferentially detected at active genes, and is proposed to promote gene expression through recognition by transcription-activating effector molecules. Here we identify a novel class of methylated H3K4 effector domains--the PHD domains of the ING (for inhibitor of growth) family of tumour suppressor proteins. The ING PHD domains are specific and highly robust binding modules for H3K4me3 and H3K4me2. ING2, a native subunit of a repressive mSin3a-HDAC1 histone deacetylase complex, binds with high affinity to the trimethylated species. In response to DNA damage, recognition of H3K4me3 by the ING2 PHD domain stabilizes the mSin3a-HDAC1 complex at the promoters of proliferation genes. This pathway constitutes a new mechanism by which H3K4me3 functions in active gene repression. Furthermore, ING2 modulates cellular responses to genotoxic insults, and these functions are critically dependent on ING2 interaction with H3K4me3. Together, our findings establish a pivotal role for trimethylation of H3K4 in gene repression and, potentially, tumour suppressor mechanisms.
955 citations
TL;DR: It is reported here that mSin3A is an in vivo component of large, heterogeneous multiprotein complexes and is tightly and specifically associated with at least seven polypeptides and histone deacetylation mediates transcriptional repression through Mad-Max-m Sin3A multimeric complexes.
756 citations
TL;DR: In vivo transactivation assays suggest that Myc-Max and Mad-Max complexes have opposing functions in transcription and that Max plays a central role in this network of transcription factors.
700 citations
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TL;DR: The surface of nucleosomes is studded with a multiplicity of modifications that can dictate the higher-order chromatin structure in which DNA is packaged and can orchestrate the ordered recruitment of enzyme complexes to manipulate DNA.
10,046 citations
TL;DR: The work from the authors' laboratories reviewed herein was supported by grants from the National Cancer Institute.
6,895 citations
TL;DR: Overexpressed Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3-dependent cell line and counters the death repressor activity of B cl-2, suggesting a model in which the ratio of Bcl-2 to Bax determines survival or death following an apoptotic stimulus.
6,193 citations
TL;DR: The known histone modifications are described, where they are found genomically and discussed and some of their functional consequences are discussed, concentrating mostly on transcription where the majority of characterisation has taken place.
Abstract: Chromatin is not an inert structure, but rather an instructive DNA scaffold that can respond to external cues to regulate the many uses of DNA. A principle component of chromatin that plays a key role in this regulation is the modification of histones. There is an ever-growing list of these modifications and the complexity of their action is only just beginning to be understood. However, it is clear that histone modifications play fundamental roles in most biological processes that are involved in the manipulation and expression of DNA. Here, we describe the known histone modifications, define where they are found genomically and discuss some of their functional consequences, concentrating mostly on transcription where the majority of characterisation has taken place.
4,536 citations
TL;DR: The bax gene promoter region contains four motifs with homology to consensus p53-binding sites and wild-type but not mutant p53 protein bound to oligonucleotides corresponding to this region of the bax promoter, suggesting that bax is a p53 primary-response gene, presumably involved in a p 53-regulated pathway for induction of apoptosis.
4,150 citations