By Zigang Dong, Young-Joon Surh
A outcome of swift growth within the technology of nutrigenomics and nutrigenetics is the massive accumulation of information masking nutrienal modulation of gene expression on the mobile and subcellular degrees. present learn is more and more occupied with the position of meals and nutrition in enhancing oxidative harm within the development of ailment. nutritional Modulation of mobilephone Signaling Pathways studies a few of these findings, concentrating on nutrient-gene interactions with specific emphasis at the intracellular signaling network.
Explore a Pivotal functionality for keeping Homeostasis
The booklet addresses the nutritional modulation of specific gene expression platforms and highlights the underlying molecular and mobile mechanisms that contain upstream signaling molecules, comparable to kinases and transcription elements within the context in their healing strength. It describes food’ activities at the activation of an antioxidant and inflammatory transcription issue and the induction in their aim gene expression.
Provides a Mechanistic realizing of the motion of nutritional elements
Comprehensively protecting nutritional modulation of mobilephone signaling, prime specialists offer info on state of the art examine of their personal strong point. For these operating within the fields of nutritional parts, molecular mechanisms, and health and wellbeing merits, this booklet offers a great tool for mechanistic figuring out of the motion of nutritional parts.
Read Online or Download Dietary Modulation of Cell Signaling Pathways (Oxidative Stress and Disease) PDF
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Additional info for Dietary Modulation of Cell Signaling Pathways (Oxidative Stress and Disease)
N. (2002). Antioxidants and oxidants regulated signal transduction pathways. Biochem. , 64, 765–70. 18. Chen, C. N. (2004). Dietary chemopreventive compounds and ARE/ EpRE signaling. Free Radic. Biol. , 36, 1505–16. 19. S. J. (2005). Nrf2 as a novel molecular target for chemoprevention. , 224, 171–84. 20. T. (2005). CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life. Oncogene, 24, 367–80. 21. R. (1998). Increased skin tumorigenesis in mice lacking pi class glutathione S-transferases.
However, the inhibition of well-defined prosurvival pathways and induction of apoptotic signaling cascades appear as common mechanisms of chemoprevention with dietary phytochemicals. Among the cell signaling molecules, Nrf2 and HIF-1α appear as critical targets for chemoprevention. Although a direct link between Nrf2 and HIF-1α is yet to be established, existing literature suggests that targeted induction of Nrf2 and inhibition of HIF-1α by edible phytochemicals may provide molecular basis of dietary chemoprevention.
T. (2005). CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life. Oncogene, 24, 367–80. 21. R. (1998). Increased skin tumorigenesis in mice lacking pi class glutathione S-transferases. Proc. Natl. Acad. Sci. USA, 95, 5275–80. 22. , and St Clair, D. (2001). Overexpression of manganese superoxide dismutase suppresses tumor formation by modulation of activator protein-1 signaling in a multistage skin carcinogenesis model. , 61, 6082–8. 23. F.