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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SCO2 induces p53-mediated apoptosis by Thr845 phosphorylation of ASK-1 and dissociation of the ASK-1-Trx complex.
TL;DR: It is proposed that SCO2 might possess a novel tumor suppressor function via the ROS–ASK-1 kinase pathway and thus could be an important candidate for anticancer gene therapy.
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Hypoglycemia Enhances Epithelial-Mesenchymal Transition and Invasiveness, and Restrains the Warburg Phenotype, in Hypoxic HeLa Cell Cultures and Microspheroids
Alvaro Marín-Hernández,Juan Carlos Gallardo-Pérez,Ileana Hernández-Reséndiz,Isis Del Mazo-Monsalvo,Diana Xochiquetzal Robledo-Cadena,Rafael Moreno-Sánchez,Sara Rodríguez-Enríquez +6 more
TL;DR: Observations indicate that HH cancer cells develop an attenuated Warburg and pronounced EMT‐ and invasive‐phenotype and the glycolytic inhibitors iodoacetate and gossypol were more effective than mitochondrial inhibitors in decreasing HH‐cancer cell viability.
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The role of metabolic therapy in treating glioblastoma multiforme
TL;DR: The calorie restricted ketogenic diet (CR-KD) is discussed as a promising potential adjunctive metabolic therapy for patients with GBMs and the “Warburg Effect” of cancer metabolism and the microenvironment of GBM tumors is explained.
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p53 attenuates acetaminophen-induced hepatotoxicity by regulating drug-metabolizing enzymes and transporter expression
Jiahong Sun,Yajie Wen,Yanying Zhou,Yiming Jiang,Yixin Chen,Huizheng Zhang,Lihuan Guan,Xinpeng Yao,Min Huang,Huichang Bi +9 more
TL;DR: This study is the first to demonstrate the protective role of p53 in regulating APAP metabolism and disposition, which provides a potential new therapeutic target for APAP-induced liver injury.
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Senescence-inducing stress promotes proteolysis of phosphoglycerate mutase via ubiquitin ligase Mdm2
Takumi Mikawa,Takeshi Maruyama,Koji Okamoto,Hitoshi Nakagama,Matilde E. Lleonart,Takeshi Tsusaka,Kousuke Hori,Itsuo Murakami,Taisuke Izumi,Akifumi Takaori-Kondo,Masayuki Yokode,Gordon Peters,David Beach,Hiroshi Kondoh +13 more
TL;DR: Mdm2, a ubiquitin ligase and downstream effector of p53, attenuates the proliferative potential of primary cells via ubiquitination and degradation of the glycolytic enzyme PGAM under senescence-inducing stress.
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.