Donald E. Ayer, PhD
- Thioredoxin Interacting Protein
- Nutrient Sensing
- Cancer Metabolism
- Departments: Oncological Sciences - Professor
- Cancer Center Programs: Nuclear Control of Cell Growth & Differentiation
Academic Office Information
Huntsman Cancer Institute
2000 Circle of Hope, Room: 3705
Salt Lake City, UT 84112
Donald Ayer, PhD, is an investigator at Huntsman Cancer Institute (HCI) and a professor in the Department of Oncological Sciences at the University of Utah (U of U). He is a member of the Nuclear Control of Cell Growth and Differentiation Program.
Ayer is a leader in the area of gene regulation and its role in normal and cancer cell growth. His research focuses on how cells regulate a transcription factor known as Myc, which is mutated in a wide variety of cancers. In normal cells, Myc is responsible for turning on the genes that are required for cell division. In cancer cells, Myc is "hyperactive" and causes cells to divide continuously, creating excess, unnecessary cells that form a tumor. Ayer's research group investigates how Myc functions in normal and cancer cells, and they work to increase the understanding of basic gene control mechanisms. This information could greatly improve cancer diagnosis methods and treatment.
Ayer, a native of Michigan, earned a PhD in chemistry and biochemistry from the University of Colorado. From 1989 to 1995, he received additional training under the direction of Robert Eisenman, PhD, a National Academy of Science member, at the Fred Hutchinson Cancer Research Center in Seattle. In 1995, he was recruited to the U of U and HCI.
|Postdoctoral Fellowship||Fred Hutchinson Cancer Research Center
|Doctoral Training||University of Colorado
Chemistry & Biochemistry
|Undergraduate||University of Michigan
Cellular and Molecular Biology
- Ahn B, Wan S, Jaiswal N, Vega RB, Ayer DE, Titchenell PM, Han X, Won KJ, Kelly DP (2019). MondoA drives muscle lipid accumulation and insulin resistance. JCI Insight, 5.
- Wilde BR, Ye Z, Lim TY, Ayer DE (2019). Cellular acidosis triggers human MondoA transcriptional activity by driving mitochondrial ATP production. eLife, 8.
- Ye Z, Ayer DE (2018). Ras Suppresses TXNIP Expression by Restricting Ribosome Translocation. Mol Cell Biol, 38(20).
- Sullivan WJ, Mullen PJ, Schmid EW, Flores A, Momcilovic M, Sharpley MS, Jelinek D, Whiteley AE, Maxwell MB, Wilde BR, Banerjee U, Coller HA, Shackelford DB, Braas D, Ayer DE, de Aguiar Vallim TQ, Lowry WE, Christofk HR (2018). Extracellular Matrix Remodeling Regulates Glucose Metabolism through TXNIP Destabilization. Cell, 175(1), 117-132.e21.
- Schaub FX, Dhankani V, Berger AC, Trivedi M, Richardson AB, Shaw R, Zhao W, Zhang X, Ventura A, Liu Y, Ayer DE, Hurlin PJ, Cherniack AD, Eisenman RN, Bernard B, Grandori C, Cancer Genome Atlas Network (2018). Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas. Cell Syst, 6(3), 282-300.e2.
- Wilde BR, Ayer DE (2015). Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis. Br J Cancer, 113(11), 1529-33.
- Shen L, OShea JM, Kaadige MR, Cunha S, Wilde BR, Cohen AL, Welm AL, Ayer DE (2015). Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP. Proc Natl Acad Sci U S A, 112(17), 5425-30.
- Carroll PA, Diolaiti D, McFerrin L, Gu H, Djukovic D, Du J, Cheng PF, Anderson S, Ulrich M, Hurley JB, Raftery D, Ayer DE, Eisenman RN (2015). Deregulated Myc requires MondoA/Mlx for metabolic reprogramming and tumorigenesis. Cancer Cell, 27(2), 271-85.
- Kaadige MR, Yang J, Wilde BR, Ayer DE (2015). MondoA-Mlx transcriptional activity is limited by mTOR-MondoA interaction. Mol Cell Biol, 35(1), 101-10.
- Bowman CJ, Ayer DE, Dynlacht BD (2014). Foxk proteins repress the initiation of starvation-induced atrophy and autophagy programs. Nat Cell Biol, 16(12), 1202-14.
- Parmenter TJ, Kleinschmidt M, Kinross KM, Bond ST, Li J, Kaadige MR, Rao A, Sheppard KE, Hugo W, Pupo GM, Pearson RB, McGee SL, Long GV, Scolyer RA, Rizos H, Lo RS, Cullinane C, Ayer DE, Ribas A, Johnstone RW, Hicks RJ, McArthur GA (2014). Response of BRAF-mutant melanoma to BRAF inhibition is mediated by a network of transcriptional regulators of glycolysis. Cancer Discov, 4(4), 423-33.
- OShea JM, Ayer DE (2013). Coordination of nutrient availability and utilization by MAX- and MLX-centered transcription networks. Cold Spring Harb Perspect Med, 3(9), a014258.
- Han KS, Ayer DE (2013). MondoA senses adenine nucleotides: transcriptional induction of thioredoxin-interacting protein. Biochem J, 453(2), 209-18.
- Stoltzman CA, Kaadige MR, Peterson CW, Ayer DE (2011). MondoA senses non-glucose sugars: regulation of thioredoxin-interacting protein (TXNIP) and the hexose transport curb. J Biol Chem, 286(44), 38027-34.
- Peterson CW, Ayer DE (2011). An extended Myc network contributes to glucose homeostasis in cancer and diabetes. Front Biosci, 16, 2206-23.
- Chen JL, Merl D, Peterson CW, Wu J, Liu PY, Yin H, Muoio DM, Ayer DE, West M, Chi JT (2010). Lactic acidosis triggers starvation response with paradoxical induction of TXNIP through MondoA. PLoS Genet, 6(9), e1001093.
- Elgort MG, OShea JM, Jiang Y, Ayer DE (2010). Transcriptional and Translational Downregulation of Thioredoxin Interacting Protein Is Required for Metabolic Reprogramming during G(1). Genes Cancer, 1(9), 893-907.
- Kaadige MR, Elgort MG, Ayer DE (2010). Coordination of glucose and glutamine utilization by an expanded Myc network. Transcription, 1(1), 36-40.
- Sloan EJ, Ayer DE (2010). Myc, mondo, and metabolism. Genes Cancer, 1(6), 587-96.
- Peterson CW, Stoltzman CA, Sighinolfi MP, Han KS, Ayer DE (2010). Glucose controls nuclear accumulation, promoter binding, and transcriptional activity of the MondoA-Mlx heterodimer. Mol Cell Biol, 30(12), 2887-95.
- Kaadige MR, Looper RE, Kamalanaadhan S, Ayer DE (2009). Glutamine-dependent anapleurosis dictates glucose uptake and cell growth by regulating MondoA transcriptional activity. Proc Natl Acad Sci U S A, 106(35), 14878-83.
- Silveira AC, Hurst DR, Vaidya KS, Ayer DE, Welch DR (2009). Over-expression of the BRMS1 family member SUDS3 does not suppress metastasis of human cancer cells. Cancer Lett, 276(1), 32-7.
- Stoltzman CA, Peterson CW, Breen KT, Muoio DM, Billin AN, Ayer DE (2008). Glucose sensing by MondoA:Mlx complexes: a role for hexokinases and direct regulation of thioredoxin-interacting protein expression. Proc Natl Acad Sci U S A, 105(19), 6912-7.
- Hassig CA, Fleischer TC, Billin AN, Schreiber SL, Ayer DE (1997). Histone deacetylase activity is required for full transcriptional repression by mSin3A. Cell, 89(3), 341-7.
- Ayer DE, Lawrence QA, Eisenman RN (1995). Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3. Cell, 80(5), 767-776.
- Ayer DE, Eisenman RN (1993). A switch from Myc:Max to Mad:Max heterocomplexes accompanies monocyte/macrophage differentiation. Genes Dev, 7(11), 2110-9.
- Ayer DE, Kretzner L, Eisenman RN (1993). Mad: a heterodimeric partner for Max that antagonizes Myc transcriptional activity. Cell, 72(2), 211-22.