TIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis
Karim Bensaad,Atsushi Tsuruta,Mary A. Selak,M. Nieves Calvo Vidal,Katsunori Nakano,Ramon Bartrons,Eyal Gottlieb,Karen H. Vousden +7 more
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TLDR
expression of TIGAR may modulate the apoptotic response to p53, allowing survival in the face of mild or transient stress signals that may be reversed or repaired, and the decrease of intracellular ROS levels in response to TIGar may also play a role in the ability of p53 to protect from the accumulation of genomic damage.About:
This article is published in Cell.The article was published on 2006-07-14 and is currently open access. It has received 1803 citations till now. The article focuses on the topics: TP53-inducible glycolysis and apoptosis regulator & Apoptosis Regulator.read more
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The Regulation of Energy Metabolism and the IGF-1/mTOR Pathways by the p53 Protein
TL;DR: Two additional functions of p53 in the regulation of IGF-1/AKT/mTOR pathways and energy metabolism are revealed, contributing to p53's role as a tumor suppressor.
Journal ArticleDOI
Cell-permeating alpha-ketoglutarate derivatives alleviate pseudohypoxia in succinate dehydrogenase-deficient cells.
Elaine D. MacKenzie,Mary A. Selak,Daniel A. Tennant,Lloyd J. Payne,Stuart Crosby,Casper M. Frederiksen,David G. Watson,Eyal Gottlieb +7 more
TL;DR: This study shows that succinate- or fumarate-mediated inhibition of PHD is competitive and is reversed by pharmacologically elevating intracellular α-ketoglutarate, indicating new therapy possibilities for the cancers associated with TCA cycle dysfunction.
Journal ArticleDOI
Reactive oxygen species in skeletal muscle signaling.
Elena Barbieri,Piero Sestili +1 more
TL;DR: A specific threshold of physiological ROS concentrations above which ROS exert negative, toxic effects is hard to determine, and the concept of “physiologically compatible” levels of ROS would better fit with such a dynamic scenario.
Journal ArticleDOI
mTOR Complex 2 Controls Glycolytic Metabolism in Glioblastoma through FoxO Acetylation and Upregulation of c-Myc
Kenta Masui,Kazuhiro Tanaka,David Akhavan,Ivan Babic,Beatrice Gini,Tomoo Matsutani,Akio Iwanami,Feng Liu,Genaro R. Villa,Genaro R. Villa,Yuchao Gu,Yuchao Gu,Carl Campos,Shaojun Zhu,Huijun Yang,William H. Yong,Timothy F. Cloughesy,Ingo K. Mellinghoff,Webster K. Cavenee,Webster K. Cavenee,Reuben J. Shaw,Reuben J. Shaw,Paul S. Mischel,Paul S. Mischel +23 more
TL;DR: It is shown that mTORC2 promotes inactivating phosphorylation of class IIa histone deacetylases, which leads to the acetylation of FoxO1 and FoxO3, and this in turn releases c-Myc from a suppressive miR-34c-dependent network.
Journal ArticleDOI
Autophagy in idiopathic pulmonary fibrosis.
Avignat Patel,Ling Lin,Alexander Geyer,Jeffrey A. Haspel,Chang Hyeok An,Jiaofei Cao,Ivan O. Rosas,Ivan O. Rosas,Danielle Morse +8 more
TL;DR: Impairment of autophagy by TGF-β1 may represent a mechanism for the promotion of fibrogenesis in IPF because it leads to the opposite effect on fibroblast expression of á-smooth muscle actin and fibronectin.
References
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Surfing the p53 network
TL;DR: The p53 tumour-suppressor gene integrates numerous signals that control cell life and death, and the disruption of p53 has severe consequences when a highly connected node in the Internet breaks down.
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In vivo activation of the p53 pathway by small-molecule antagonists of MDM2.
Lyubomir T. Vassilev,Binh Thanh Vu,Bradford Graves,Daisy Carvajal,Frank John Podlaski,Zoran Filipovic,Norman Kong,Ursula Kammlott,Christine Lukacs,Christian Klein,Nader Fotouhi,Liu Emily Aijun +11 more
TL;DR: In this article, the authors identify potent and selective small-molecule antagonists of MDM2 and confirm their mode of action through the crystal structures of complexes, leading to cell cycle arrest, apoptosis, and growth inhibition of human tumor xenografts.
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Live or let die: the cell's response to p53
Karen H. Vousden,Xin Lu +1 more
TL;DR: Understanding the complex mechanisms that regulate whether or not a cell dies in response to p53 will ultimately contribute to the development of therapeutic strategies to repair the apoptotic p53 response in cancers.