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 Warburg effect and mitochondrial stability in cancer cells
TL;DR: Potential mechanisms underlying the upregulation of glycolysis and silencing of mitochondrial activity in cancer cells are discussed, and how pharmaceutical intervention in cellular energy metabolism might make tumor cells more susceptible to anti-cancer treatment is discussed.
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The circadian clock in cancer development and therapy
Loning Fu,Nicole M. Kettner +1 more
TL;DR: The hierarchical mammalian circadian clock provides a unique system to study carcinogenesis as a deregulated physiological process in vivo and provides new and exciting options for novel anticancer therapies.
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Endoplasmic Reticulum Stress, the Unfolded Protein Response, Autophagy, and the Integrated Regulation of Breast Cancer Cell Fate
Robert Clarke,Katherine L. Cook,Rong Hu,Caroline O. B. Facey,Iman Tavassoly,Jessica L. Schwartz,William T. Baumann,John J. Tyson,Jianhua Xuan,Yue Wang,Anni Wärri,Ayesha N. Shajahan +11 more
TL;DR: The unfolded protein response, autophagy, and apoptosis are described, and how the regulation of these processes is integrated are discussed.
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Apoptosis-induced mitochondrial dysfunction causes cytoplasmic lipid droplet formation
Joan Boren,Kevin M. Brindle +1 more
TL;DR: It is shown that despite an apoptosis-induced decrease in the levels and activities of enzymes involved in lipogenesis, which occurs downstream of p53 activation and inhibition of the mTOR signaling pathway, the increase in lipid accumulation is due to increased de novo lipid synthesis.
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Role of mitochondrial dysfunction in cancer progression
TL;DR: It is suggested that mitochondrial dysfunction plays a critical role in cancer progression and that targeting mitochondrial alterations and mitochondrial retrograde signaling might be a promising strategy for the development of selective anticancer therapy.
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.