Research summary
Nuclear receptor biology, lipid sensing, and the tumor microenvironment form the connective tissue of this research output. A 1988 Science article framed steroid receptor analyses as a route to molecular dissection of transcriptional control and cell identity, and reported the identification of a regulatory protein superfamily that includes receptors for steroids, thyroid hormone, and the morphogen retinoic acid; the broad species distribution of related molecules implied conserved roles in morphogenesis and homeostasis [1]. A 2020 Nature Reviews Cancer consensus piece synthesized expert discussion on cancer-associated fibroblasts (CAFs), describing their roles in matrix deposition and remodeling, reciprocal signaling with cancer cells, and crosstalk with infiltrating leukocytes, and proposing a framework for therapeutic targeting that preserves potentially beneficial antitumorigenic CAF functions while accounting for cell-of-origin and functional heterogeneity [2]. A 1997 PNAS study addressed how structurally diverse lipid-like compounds activate a single nuclear receptor: using a conformation-based DNA-binding assay, it demonstrated that specific fatty acids, eicosanoids, and hypolipidemic drugs serve as direct ligands for peroxisome proliferator-activated receptors alpha and delta (PPARalpha and PPARdelta), establishing these receptors as sensors of cellular lipid status that link nutrient flux to transcriptional programs governing lipid homeostasis [3]. A 2001 Science review titled "Nuclear Receptors and Lipid Physiology: Opening the X-Files" integrated these threads into a wider model in which dietary cholesterol, fatty acids, fat-soluble vitamins, and other lipids must be absorbed, enzymatically transformed into bioactive ligands, distributed to target tissues, and ultimately cleared to preserve homeostasis [4]. The review emphasized the coordination problems posed by such a multistep signaling cascade and the regulatory logic by which nuclear receptors couple lipid metabolism to absorption, distribution, and elimination. Taken together, the four works trace a coherent program: defining a receptor superfamily, identifying the endogenous and pharmacological ligands that activate its lipid-sensing members, situating that signaling within whole-body lipid physiology, and extending the framework to stromal cell populations relevant in cancer.
Recent publications
- The Steroid and Thyroid Hormone Receptor SuperfamilyDOI
- The nuclear receptor superfamily: The second decadeDOI
- A framework for advancing our understanding of cancer-associated fibroblastsDOI
- The RXR heterodimers and orphan receptorsDOI
- 15-Deoxy-螖12,14-Prostaglandin J2 is a ligand for the adipocyte determination factor PPAR纬DOI
- Production of a novel neuropeptide encoded by the calcitonin gene via tissue-specific RNA processingDOI
- Alternative RNA processing in calcitonin gene expression generates mRNAs encoding different polypeptide productsDOI
- Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors 伪 and 未DOI
- Nuclear Receptors and Lipid Physiology: Opening the X-FilesDOI
- Identification of a receptor for the morphogen retinoic acidDOI
The lab page does not clearly state student acceptance status. Email the professor directly to confirm.
How to apply
Email Ronald M. Evans 6-12 months before your application deadline. Read several recent papers and reference specific work in your message. Use our how to email a Japanese professor guide for the proven email structure.
For applications via MEXT scholarship: see our MEXT 2027 complete guide and university-specific University Recommendation track.
External profiles
- ORCID: https://orcid.org/0000-0002-9986-5965
- OpenAlex: openalex.org
Profile compiled from public sources (Researchmap, OpenAlex, The University of Tokyo faculty directory). Last refreshed 2026-05. Report incorrect information.