Lorenzo Galluzzi; Guido Kroemer; Woo Suk Ahn's Methods in enzymology. Volume five hundred and forty two, PDF

By Lorenzo Galluzzi; Guido Kroemer; Woo Suk Ahn

ISBN-10: 0124166180

ISBN-13: 9780124166189

ISBN-10: 0124166571

ISBN-13: 9780124166578

Quantity 542 of Methods in Enzymology keeps the legacy of this most appropriate serial with caliber chapters authored via leaders within the box. This new quantity covers examine equipment offering a theoretical review on metabolic changes of melanoma cells and a sequence of protocols that may be hired to review oncometabolism, in vitro, ex vivo and in vivo. Malignant cells show metabolic alterations compared to their basic opposite numbers, due to either genetic and epigenetic adjustments. even if this kind of metabolic rewiring has lately been indicated as ''yet another'' common hallmark of melanoma, gathering proof means that the metabolic adjustments of every neoplasm really signify a molecular signature that in detail accompanies, and for that reason can't be severed from, all features of malignant transformation.

  • Continues the legacy of this superior serial with caliber chapters authored by way of leaders within the box
  • Covers examine tools in biomineralization science
  • Provides theoretical evaluation on metabolic changes of melanoma cells, and a sequence of protocols that may be hired to review oncometabolism, in vitro, ex vivo and in vivo

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Extra resources for Methods in enzymology. Volume five hundred and forty two, Conceptual background and bioenergetic/mitochondrial aspects of oncometabolism

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MacKenzie, E. , Watson, D. , Mansfield, K. , et al. (2005). Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-alpha prolyl hydroxylase. Cancer Cell, 7(1), 77–85. , Lewis, B. , Wu, C. , Jungmann, R. , et al. (1997). c-Myc transactivation of LDH-a: Implications for tumor metabolism and growth. Proceedings of the National Academy of Sciences of the United States of America, 94(13), 6658–6663. Sugiura, Kanematsu, & Benedict, Stanley R. (1929). The action of certain dyestuffs on the growth of transplantable tumors.

2006; Qin, Wang, Tao, & Wang, 2010; Tomohiro & Klionsky, 2007). 6. Hypoxia and ROS Hypoxia and ROS, often found in the poorly vascularized tumor microenvironment, have been shown to increase autophagic flux via several mechanisms. , 2007). , 2009). AMPK promotes autophagy independently of HIF in response to severe hypoxia. While BNIP3-regulated autophagy protects cells from death, AMPK-induced autophagy promotes cell death, pointing 36 Juliet Goldsmith et al. to the influence of cellular context on the outcome of autophagy (Papandreou, Lim, Laderoute, & Denko, 2008).

Science, 334(6060), 1278–1283. , & Loda, M. (2004). Fatty acid synthase: A metabolic oncogene in prostate cancer? Journal of Cellular Biochemistry, 91(1), 47–53. Baysal, B. , Ferrell, R. , Willett-Brozick, J. , Lawrence, E. , et al. (2000). Mutations in SDHD, a mitochondrial complex II gene, in hereditary paraganglioma. Science, 287(5454), 848–851. , & Swinnen, J. V. (2005). RNA interference-mediated silencing of the acetyl-CoA-carboxylase-alpha gene induces growth inhibition and apoptosis of prostate cancer cells.

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Methods in enzymology. Volume five hundred and forty two, Conceptual background and bioenergetic/mitochondrial aspects of oncometabolism by Lorenzo Galluzzi; Guido Kroemer; Woo Suk Ahn


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