By Zigang Dong, Young-Joon Surh
A outcome of swift growth within the technological know-how of nutrigenomics and nutrigenetics is the great accumulation of knowledge protecting nutrienal modulation of gene expression on the mobile and subcellular degrees. present examine is more and more concerned about the function of food and nutrition in enhancing oxidative harm within the development of sickness. nutritional Modulation of telephone Signaling Pathways stories a few of these findings, concentrating on nutrient-gene interactions with specific emphasis at the intracellular signaling network.
Explore a Pivotal functionality for retaining Homeostasis
The booklet addresses the nutritional modulation of specific gene expression structures and highlights the underlying molecular and mobile mechanisms that contain upstream signaling molecules, corresponding to kinases and transcription elements within the context in their healing capability. It describes nutrition’ activities at the activation of an antioxidant and inflammatory transcription issue and the induction in their goal gene expression.
Provides a Mechanistic knowing of the motion of nutritional parts
Comprehensively protecting nutritional modulation of phone signaling, best specialists supply info on state of the art study of their personal forte. For these operating within the fields of nutritional elements, molecular mechanisms, and overall healthiness merits, this ebook provides a great tool for mechanistic knowing of the motion of nutritional elements.
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Additional resources for Dietary Modulation of Cell Signaling Pathways (Oxidative Stress and Disease)
Example text
Several studies have reported that HIF-2α is upregulated in tumor parenchymal cells and in tumor-associated macrophages (TAM), which are recruited to the hypoxic, avascular regions of tumors by growth factors and chemokines resulting in tumor progression [81,85,86]. A number of HIF-regulated angiogenic factors, such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), VEGF receptor (VEGFR), IL-8, iNOS, and angiopoietins, are released by macrophages [81,87]. Many of these factors further accelerate inflammatory angiogenic process, thereby triggering tumor growth [88].
Indd 8 8/21/2008 3:23:27 PM Signaling Molecules as Targets of Dietary Chemopreventives 9 abnormally proliferating cells that comprise premalignant or malignant tumors by the modulation of cell cycle progression is another important strategy for chemoprevention as well as therapy [4,66]. A cell cycle consists of four different phases: gap I (G1), synthesis (S), gap 2 (G2), and mitosis (M). During the G1 phase, cells grow in size and get prepared for DNA replication. The S phase involves the replication of chromosomes, and the G2 phase checks the completion of DNA replication and prepares cells to undergo mitosis.
Capsaicin induced apoptosis in HL-60 cells, human esophagus epidermoid carcinoma cells, and B16-F10 melanoma cells, which was accompanied by the decrease in levels of mitochondrial membrane potential, enhanced cytochrome c release, and increased activation of caspase-3 [255,257,258]. Treatment of HT-29 cells with capsaicin caused apoptosis via upregulation of AMPK [259]. Capsaicin caused G1 arrest in endothelial cells that was correlated with the downregulation of the expression of cyclin D1-Cdk-4 and reduced phosphorylation of Rb protein.
