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. Author manuscript; available in PMC: 2012 Oct 1.
Published in final edited form as: J Pineal Res. 2011 May 24;51(3):259–269. doi: 10.1111/j.1600-079X.2011.00888.x

Figure 1.

Figure 1

Impact of the nocturnal circadian melatonin signal, via the MT1 receptor, and its disruption by LAN on molecular/endocrine and dietary/metabolic regulatory mechanisms governing breast cancer initiation, growth promotion and progression. Abbreviations used are: 13-HODE (13-hydroxyoctadecadienoic acid), 17βHSD (17β-hydroxysteroid dehydrogenase), Akt (Serine/Threonine Protein Kinase), Bax (Bcl-2-Associated × Protein), BMAL1 (Brain and Muscle Aryl Hydrocarbon Receptor Nuclear Translocator – Like 1), BRCA 1 & 2 (Breast Cancer 1 & 2), CLOCK (Circadian Locomotor Output Cycles Kaput), EGFR (Epidermal Growth Factor Receptor), ERα (Estrogen Receptor Alpha), Erk (Extracellular Signal-Regulated Kinase), ERRα (Estrogen Related Receptor Alpha), EST (Estrogen Sulfotransferase), IGF-1R (Insulin-like Growth Factor-1 Receptor), MMP (Matrix Metalloproteinase), MT1 (Melatonin Receptor 1), Per 1, 2 (Period 1, 2), PGC1α (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha), PPARγ (Peroxisome Proliferator-Activated Receptor Protein Gamma), RARα (Retinoic Acid Receptor Alpha), Rev-erbα (aka NR1D1, Nuclear Receptor Subfamily 1, group D, member 1), RORα (RAR-related Orphan Receptor Alpha), R×Rα (Retinoid × Receptor Alpha), SIRT1 [Sirtuin (Silent Mating Type Regulation 2 Homolog) 1], STS (Estrogen Sulfatase). Figure adapted and modified from reference [19].