Inositol pyrophosphates regulate cell death and telomere length through phosphoinositide 3-kinase-related protein kinases

Adolfo Saiardi; Adam C. Resnick; Adele M. Snowman; Beverly Wendland; Solomon H. Snyder

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Inositol pyrophosphates regulate cell death and telomere length through phosphoinositide 3-kinase-related protein kinases

机译：肌醇焦磷酸盐通过磷酸肌醇3-激酶相关的蛋白激酶调节细胞死亡和端粒长度

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Inositol pyrophosphates physiologically regulate vesicular endo-cytosis, ribosomal disposition, and directly phosphorylate proteins. Here we demonstrate roles in cell death and regulation of telomere length. Lethal actions of wortmannin and caffeine are selectively abolished in yeast mutants that cannot synthesize inositol pyrophosphates. Wortmannin and caffeine appear to act through the phosphoinositide 3-kinase-related protein kinases Tel1 and Mec1, known regulators of telomere length. Inositol pyrophosphates physiologically antagonize the actions of these kinases, which is demonstrated by the fact that yeast mutants with reduced or elevated levels of inositol pyrophosphates, respectively, display longer and shorter telomeres.

机译：肌醇焦磷酸盐在生理上调节水泡内吞作用，核糖体的分布并直接磷酸化蛋白质。在这里，我们展示了细胞死亡和端粒长度调节中的作用。在不能合成肌醇焦磷酸盐的酵母突变体中，渥曼青霉素和咖啡因的致死作用被选择性地消除。 Wortmannin和咖啡因似乎通过磷酸肌醇3激酶相关的蛋白激酶Tel1和Mec1起作用，这是端粒长度的已知调节剂。肌醇焦磷酸盐在生理上拮抗这些激酶的作用，事实证明，分别具有降低或升高的肌醇焦磷酸盐水平的酵母突变体显示更长或更短的端粒。

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来源
《Proceedings of the National Academy of Sciences of the United States of America》 |2005年第6期|p.1911-1914|共4页
作者
Adolfo Saiardi; Adam C. Resnick; Adele M. Snowman; Beverly Wendland; Solomon H. Snyder;
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作者单位

Medical Research Council Laboratory for Molecular Cell Biology and Cell Biology Unit, University College London, Gower Street, London WC1E 6BT, United Kingdom;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种 eng
中图分类自然科学总论;
关键词
wortmannin; yeast; caffeine;

机译：渥曼青霉素;酵母;咖啡因;

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1. Bone marrow stromal cells increase astrocyte survival via upregulation of phosphoinositide 3-kinase/threonine protein kinase and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase pathways and stimulate astrocyte trophic fa [J] . Gao Q, Li Y, Chopp M Neuroscience: An International Journal under the Editorial Direction of IBRO . 2005,第1期

机译：骨髓基质细胞可通过上调磷酸肌醇3激酶/苏氨酸蛋白激酶和有丝分裂原激活的蛋白激酶激酶/细胞外信号调节的激酶途径来增加星形胶质细胞的存活，并刺激星形胶质细胞营养
2. Inositol pyrophosphates modulate cell cycle independently of alteration in telomere length [J] . Hrvoje Banfic, Vladiana Crljen, Vesna Lukinovic-Skudar, Advances in biological regulation . 2015,第Null期

机译：肌醇焦磷酸盐独立于端粒长度的改变而调节细胞周期
3. Silencer of Death Domains (SODD) Inhibits Skeletal Muscle and Kidney Enriched Inositol 5-Phosphatase (SKIP) and Regulates Phosphoinositide 3-Kinase (PI3K)/Akt Signaling to the Actin Cytoskeleton [J] . Parvin Rahman, Richard Huysmans, Fenny Wiradjaja, The Journal of biological chemistry . 2011,第34期

机译：死亡域（SODD）的消化剂抑制骨骼肌和肾富含肌醇5-磷酸酶（跳过），并调节磷酸膦腈3-激酶（PI3K）/ akt信号传导至肌动蛋白细胞骨架
4. Attenuation of neuronal cell death by SOD1 is associated with extracellular signal-regulated kinase after transient focal cerebral ischemia in mice [C] . Nobuo Noshita, Takeshi Hayashi, Atsushi Saito, International Symposium on Molecular Mechanism and Epochal Therapeutics for Ischemic Stroke and Dementia . 2003

机译：SOD1的神经元细胞死亡的衰减与小鼠瞬时焦点脑缺血后细胞外信号调节激酶有关
5. Inositol (1,4,5) trisphosphate 3-kinase B (ItpkB) is central to thymic development by regulating Phosphoinositide 3-kinase (PI3K) downstream of mild and strong TCR signals. [D] . Sternberg, Luise. 2013

机译：肌醇（1,4,5）三磷酸3激酶B（ItpkB）通过调节轻度和强TCR信号下游的磷酸肌醇3激酶（PI3K）对胸腺发育至关重要。
6. From the Cover: Inositol pyrophosphates regulate cell death and telomere length through phosphoinositide 3-kinase-related protein kinases [O] . Adolfo Saiardi, Adam C. Resnick, Adele M. Snowman, 2005

机译：从封面开始：肌醇焦磷酸盐通过磷酸肌醇3-激酶相关的蛋白激酶调节细胞死亡和端粒长度
7. Inositol pyrophosphates regulate cell death and telomere length through phosphoinositide 3-kinase-related protein kinases [O] . Saiardi, Adolfo, Resnick, Adam C., Snowman, Adele M., 2005

机译：肌醇焦磷酸盐通过磷酸肌醇3-激酶相关的蛋白激酶调节细胞死亡和端粒长度

Inositol pyrophosphates regulate cell death and telomere length through phosphoinositide 3-kinase-related protein kinases

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