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您的检索式：作者名="Laura Mondragon"
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| 1 | AIF-regulated oxidative phosphorylation supports lung cancer development显示文摘Cancer is a major and still increasing cause of death in humans. Most cancer cells have a fundamentally different metabolic profile from that of normal tissue. This shift away from mitochondrial ATP synthesis via oxidative phosphorylation towards a high rate of glycolysis, termed Warburg effect, has long been recognized as a paradigmatic hallmark of cancer, supporting the increased biosynthetic demands of tumor cells. Here we show that deletion of apoptosis-inducing factor (AIF) in a Kras^G12D-driven mouse lung cancer model resulted in a marked survival advantage, with delayed tumor onset and decreased malignant progression. Mechanistically, Aif deletion leads to oxidative phosphorylation (OXPHOS) deficiency and a switch in cellular metabolism towards glycolysis in non-transformed pneumocytes and at early stages of tumor development. Paradoxically, although Aif-deficient cells exhibited a metabolic Warburg profile, this bioenergetic change resulted in a growth disadvantage of Kras^G12D-driven as well as Kras wild-type lung cancer cells. Cell-autonomous re-expression of both wild-type and mutant AIF (displaying an intact mitochondrial, but abrogated apoptotic function) in Aif-knockout Kras^G12D mice restored OXPHOS and reduced animal survival to the same level as AIF wild-type mice. In patients with non-small cell lung cancer, high AIF expression was associated with poor prognosis. These data show that AIF-regulated mitochondrial respiration and OXPHOS drive the progression of lung cancer. | Shuan Rao Laura Mondragon Blanka Pranjic Toshikatsu Hanada Gautier Stoll Thomas Kocher Peng Zhang Alexander Jais Alexander Lercher Andreas Bergthaler Daniel Schramek Katharina Haigh Valentina Sica Marion Leduc Nazanine Modjtahedi Tsung-Pin Pai Masahiro Onji Iris Uribesalgo Reiko Hanada Ivona Kozieradzki Rubina Koglgruber Shane J. Cronin Zhigang She Franz Quehenberger Helmut Popper Lukas Kenner Jody J. Haigh Oliver Kepp Malgorzata Rak Kaican Cai Guido Kroemer Josef M. Penninger | 2019 | Cell Research2019，29，7： | 2 |
| 2 | Apaf1 inhibition promotes cell recovery From apoptosis显示文摘激活因素 1 的蛋白质 apoptotic 朊酶(Apaf1 ) 是 apoptosome 的中央部件,在 apoptosis 的内在的小径从线粒体在细胞色素 c 版本以后激活 procaspase-9 的 multiprotein 建筑群。我们开发了允许激活荧光的房间在 apoptotic 小径的不同阶段排序房间的一个重要方法并且证明在 Apaf1 的药理学抑制之上,房间从导致 doxorubicin 或导致组织缺氧的早 apoptosis 恢复到正常健康房间。禁止 Apaf1 不仅阻止 procaspase-9 激活而且推迟巨大的 mitochondrial 损坏允许房间恢复。 | Anna Gortat Monica Sancho Laura Mondragon Angel Messeguer Enrique Perez-Paya Mar Orzaez | 2015 | Protein & Cell2015，6，11： | 1 |
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