Donald E. Ayer

11.9k total citations · 4 hit papers
81 papers, 8.2k citations indexed

About

Donald E. Ayer is a scholar working on Molecular Biology, Cancer Research and Oncology. According to data from OpenAlex, Donald E. Ayer has authored 81 papers receiving a total of 8.2k indexed citations (citations by other indexed papers that have themselves been cited), including 61 papers in Molecular Biology, 13 papers in Cancer Research and 12 papers in Oncology. Recurrent topics in Donald E. Ayer's work include Genomics and Chromatin Dynamics (18 papers), Ubiquitin and proteasome pathways (15 papers) and Cancer, Hypoxia, and Metabolism (13 papers). Donald E. Ayer is often cited by papers focused on Genomics and Chromatin Dynamics (18 papers), Ubiquitin and proteasome pathways (15 papers) and Cancer, Hypoxia, and Metabolism (13 papers). Donald E. Ayer collaborates with scholars based in United States, Japan and South Africa. Donald E. Ayer's co-authors include Robert N. Eisenman, Andrew N. Billin, Stuart L. Schreiber, Christian A. Hassig, Tracey C. Fleischer, Leo Kretzner, László Nagy, Debabrata Chakravarti, Hung‐Ying Kao and Richard J. Lin and has published in prestigious journals such as Science, Cell and Proceedings of the National Academy of Sciences.

In The Last Decade

Donald E. Ayer

80 papers receiving 8.1k citations

Hit Papers

align trajectories

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

Nuclear Receptor Repression Mediated by a Complex Containing SMRT, mSin3A, and Histone Deacetylase

1997 1.1k citations László Nagy, Hung‐Ying Kao et al. Cell profile →
Histone Deacetylase Activity Is Required for Full Transcriptional Repression by mSin3A

1997 656 citations Christian A. Hassig, Tracey C. Fleischer et al. Cell profile →
Mad: A heterodimeric partner for Max that antagonizes Myc transcriptional activity

1993 609 citations Donald E. Ayer, Leo Kretzner et al. Cell profile →
Mad-max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3

1995 516 citations Donald E. Ayer, Robert N. Eisenman et al. Cell profile →

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name	h						Papers	Cites
Donald E. Ayer United States	47	6.7k	1.2k	1.2k	1.0k	591	81	8.2k
Jean‐Claude Chambard France	34	4.6k 0.7×	1.2k 1.0×	972 0.8×	1.0k 1.0×	726 1.2×	52	7.4k
Claude Cochet France	50	5.8k 0.9×	1.9k 1.6×	841 0.7×	496 0.5×	1.0k 1.7×	191	8.1k
Ralf Janknecht United States	61	8.3k 1.2×	1.7k 1.4×	964 0.8×	1.6k 1.6×	834 1.4×	125	10.2k
Barbara A. Spengler United States	42	3.9k 0.6×	1.2k 1.0×	895 0.8×	908 0.9×	685 1.2×	84	6.4k
Roseline Godbout Canada	44	4.9k 0.7×	1.7k 1.4×	1.1k 1.0×	1.5k 1.4×	439 0.7×	132	6.9k
Vincent J. Kidd United States	47	5.3k 0.8×	2.0k 1.6×	636 0.6×	1.1k 1.1×	1.1k 1.9×	100	7.2k
Jeffrey E. Kudlow United States	51	5.6k 0.8×	1.1k 0.9×	887 0.8×	758 0.7×	663 1.1×	97	7.5k
Klaus Hansen Denmark	36	6.0k 0.9×	923 0.8×	805 0.7×	805 0.8×	352 0.6×	56	7.0k
Claude Sardet France	41	6.0k 0.9×	1.2k 1.0×	471 0.4×	750 0.7×	800 1.4×	86	7.4k
Ross D. Hannan Australia	53	6.4k 1.0×	1.4k 1.1×	430 0.4×	833 0.8×	430 0.7×	151	8.6k

Countries citing papers authored by Donald E. Ayer

Since Specialization

Citations

This map shows the geographic impact of Donald E. Ayer's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Donald E. Ayer with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Donald E. Ayer more than expected).

Fields of papers citing papers by Donald E. Ayer

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Donald E. Ayer. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Donald E. Ayer. The network helps show where Donald E. Ayer may publish in the future.

Co-authorship network of co-authors of Donald E. Ayer

This figure shows the co-authorship network connecting the top 25 collaborators of Donald E. Ayer. A scholar is included among the top collaborators of Donald E. Ayer based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Donald E. Ayer. Donald E. Ayer is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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20 of 20 papers shown

Antelope, Orlando, Donald E. Ayer, Randall T. Peterson, et al.. (2024). Bioluminescence assay of lysine deacylase sirtuin activity. Cell chemical biology. 31(11). 2002–2014.e4.

Carroll, Patrick A., Brian Freie, Pei Cheng, et al.. (2021). The glucose-sensing transcription factor MLX balances metabolism and stress to suppress apoptosis and maintain spermatogenesis. PLoS Biology. 19(10). e3001085–e3001085. 13 indexed citations

Wilde, Blake R., et al.. (2019). Cellular acidosis triggers human MondoA transcriptional activity by driving mitochondrial ATP production. eLife. 8. 40 indexed citations

Sullivan, William J., Peter Mullen, E. Schmid, et al.. (2018). Extracellular Matrix Remodeling Regulates Glucose Metabolism through TXNIP Destabilization. Cell. 175(1). 117–132.e21. 194 indexed citations

Carroll, Patrick A., Daniel Diolaiti, Lisa McFerrin, et al.. (2015). Deregulated Myc Requires MondoA/Mlx for Metabolic Reprogramming and Tumorigenesis. Cancer Cell. 27(2). 271–285. 158 indexed citations

Breen, Kevin, et al.. (2007). A C. elegans Myc-like network cooperates with semaphorin and Wnt signaling pathways to control cell migration. Developmental Biology. 310(2). 226–239. 35 indexed citations

Fleischer, Tracey C., Ui Jeong Yun, & Donald E. Ayer. (2003). Identification and Characterization of Three New Components of the mSin3A Corepressor Complex. Molecular and Cellular Biology. 23(10). 3456–3467. 143 indexed citations

Yochum, Gregory S. & Donald E. Ayer. (2002). Role for the Mortality Factors MORF4, MRGX, and MRG15 in Transcriptional Repression via Associations with Pf1, mSin3A, and Transducin-Like Enhancer of Split. Molecular and Cellular Biology. 22(22). 7868–7876. 82 indexed citations

Billin, Andrew N., et al.. (2000). MondoA, a Novel Basic Helix-Loop-Helix–Leucine Zipper Transcriptional Activator That Constitutes a Positive Branch of a Max-Like Network. Molecular and Cellular Biology. 20(23). 8845–8854. 107 indexed citations

10.

Ayer, Donald E.. (1999). Histone deacetylases: transcriptional repression with SINers and NuRDs. Trends in Cell Biology. 9(5). 193–198. 238 indexed citations

11.

McArthur, Grant A., Carol D. Laherty, Peter J. Hurlin, et al.. (1998). The Mad Protein Family Links Transcriptional Repression to Cell Differentiation. Cold Spring Harbor Symposia on Quantitative Biology. 63(0). 423–434. 49 indexed citations

12.

Laherty, Carol D., Andrew N. Billin, Gregory S. Yochum, et al.. (1998). SAP30, a Component of the mSin3 Corepressor Complex Involved in N-CoR-Mediated Repression by Specific Transcription Factors. Molecular Cell. 2(1). 33–42. 187 indexed citations

13.

Nagy, László, Hung‐Ying Kao, Debabrata Chakravarti, et al.. (1997). Nuclear Receptor Repression Mediated by a Complex Containing SMRT, mSin3A, and Histone Deacetylase. Cell. 89(3). 373–380. 1070 indexed citations breakdown →

14.

Hassig, Christian A., Tracey C. Fleischer, Andrew N. Billin, Stuart L. Schreiber, & Donald E. Ayer. (1997). Histone Deacetylase Activity Is Required for Full Transcriptional Repression by mSin3A. Cell. 89(3). 341–347. 656 indexed citations breakdown →

15.

Roussel, Martine F., Richard A. Ashmun, Charles J. Sherr, Robert N. Eisenman, & Donald E. Ayer. (1996). Inhibition of Cell Proliferation by the Mad1 Transcriptional Repressor. Molecular and Cellular Biology. 16(6). 2796–2801. 108 indexed citations

16.

Ayer, Donald E., et al.. (1995). Mad-max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3. Cell. 80(5). 767–776. 516 indexed citations breakdown →

17.

Bundy, Gordon L., Donald E. Ayer, Lee S. Banitt, et al.. (1995). Synthesis of Novel 2,4-Diaminopyrrolo[2,3-d]pyrimidines with Antioxidant, Neuroprotective, and Antiasthma Activity. Journal of Medicinal Chemistry. 38(21). 4161–4163. 48 indexed citations

18.

Hurlin, Peter J., Donald E. Ayer, Carla Grandori, & Robert N. Eisenman. (1994). The Max Transcription Factor Network: Involvement of Mad in Differentiation and an Approach to Identification of Target Genes. Cold Spring Harbor Symposia on Quantitative Biology. 59(0). 109–116. 49 indexed citations

19.

Ayer, Donald E., Leo Kretzner, & Robert N. Eisenman. (1993). Mad: A heterodimeric partner for Max that antagonizes Myc transcriptional activity. Cell. 72(2). 211–222. 609 indexed citations breakdown →

20.

Hanahan, D J, et al.. (1985). A novel approach to structure proof of glyceryl ether-containing glycerophospholipids. Base-catalyzed methanolysis of platelet-activating factor (AGEPC) at 60 degrees C. Journal of Lipid Research. 26(11). 1345–1355. 6 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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