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Ronald M. Evans

Ronald M. Evans


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Ronald M. Evans is a 2020 NOMIS Distinguished Scientist and has been a professor at the Salk Institute for Biological Studies since 1978, the director of Salk’s Gene Expression Laboratory since 1995 as well as holder of the March of Dimes Chair in Molecular and Developmental Biology since 1998. He is leading the project The Science of Health: The Fundamental Mechanisms of Organ Communication.

Evans grew up in Los Angeles, California (US) and earned a BA in bacteriology and PhD in microbiology and immunology from the University of California, Los Angeles. He completed his postdoctoral work at Rockefeller University (US) in 1978 before becoming a faculty member at Salk that same year. He has received numerous honors and awards, including the Wolf Prize in Medicine, the Albany Medical Center Prize in Medicine and Biomedical Research, the Canada Gairdner Foundation International Award, the Albert Lasker Award for Basic Medical Research, the March of Dimes Prize and the Keio Medical Science Prize. He was elected to the National Academy of Sciences in 1989 and the National Academy of Medicine in 2003.

Evans has made multiple significant contributions to science, including the discovery of a “superfamily” of molecules called nuclear hormone receptors (NRs), whose members respond to various steroid and thyroid hormones, vitamins A and D, as well as to dietary fats and bile acids. This led to the unifying theory that hormones control gene networks throughout the body, which in turn control physiologic pathways from embryonic development through adulthood. Evans has also identified multiple novel pathways involved in cancer and diabetes that are targetable by drugs that activate these receptors. More recently, he identified exercise mimetics (“exercise in a pill”), a class of drugs that stimulate gene networks in muscle tissue. By directly acting on genes, exercise mimetics confer the benefits of fitness without training — pointing to potential new therapies for children with muscular dystrophy, adults with type 2 diabetes and obese individuals. Evans is further investigating NRs to understand the mechanisms of cooperativity between interconnected networks including the brain, endocrine glands, gut, liver, immune cells and the microbiome.

Ronald M. Evans | Awards Film

Ronald M. Evans | Insights Film

Ronald M. Evans's News

NOMIS Awardee and Salk Professor Ronald Evans has been named the 2024 recipient of the Japan Prize in the field of Medical Science and Pharmaceutical Science. The Japan Prize Foundation awards […]

In an article published in Gastroenterology, NOMIS Awardee Ronald M. Evans and colleagues report that a protein known as estrogen-related receptor gamma (ERR ɣ) is critical for preventing pancreatic auto-digestion […]

Recognizing their outstanding contributions to the advancement of science and human progress through their pioneering, collaborative research, the 2021 as well as the 2020 NOMIS Distinguished Scientist and Scholar Award […]

Ronald M. Evans's Insights

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy in need of new therapeutic options. Using unbiased analyses of super-enhancers (SEs) as sentinels of core genes involved in cell-specific function, here we uncover a druggable SE-mediated RNA-binding protein (RBP) cascade that supports PDAC growth through enhanced mRNA translation. This cascade is
Abstract: Colorectal cancer (CRC) is driven by genomic alterations in concert with dietary influences, with the gut microbiome implicated as an effector in disease development and progression. While meta-analyses have provided mechanistic insight into patients with CRC, study heterogeneity has limited causal associations. Using multi-omics studies on genetically controlled cohorts of
Abstract: Molecular classification of gastric cancer (GC) identified a subgroup of patients showing chemoresistance and poor prognosis, termed SEM (Stem-like/Epithelial-to-mesenchymal transition/Mesenchymal) type in this study. Here, we show that SEM-type GC exhibits a distinct metabolic profile characterized by high glutaminase (GLS) levels. Unexpectedly, SEM-type GC cells are resistant to glutaminolysis inhibition.
Abstract: Retinoid-related orphan receptor (RAR) gamma (RORγt)-expressing regulatory T cells (RORγt+ Tregs) play pivotal roles in preventing T cell hyperactivation and maintaining tissue homeostasis, in part by secreting the anti-inflammation cytokine interleukin-10 (IL-10). Here, we report that hypoxia-induced factor 1α (HIF1α) is the master transcription factor for Il10 in RORγt+ Tregs.