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1
New insights into the generation and role of de novo mutations in health and disease.关于新生突变在健康与疾病中的产生及其作用的新见解。
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2
Somatic overgrowth disorders of the PI3K/AKT/mTOR pathway & therapeutic strategies.PI3K/AKT/mTOR通路的体细胞过度生长障碍及治疗策略。
Am J Med Genet C Semin Med Genet. 2016 Dec;172(4):402-421. doi: 10.1002/ajmg.c.31531. Epub 2016 Nov 18.
3
A four-gene signature predicts survival in clear-cell renal-cell carcinoma.一种四基因特征可预测透明细胞肾细胞癌的生存率。
Oncotarget. 2016 Dec 13;7(50):82712-82726. doi: 10.18632/oncotarget.12631.
4
Neurocutaneous Manifestations of Genetic Mosaicism.遗传性嵌合体的神经皮肤表现。
J Pediatr Genet. 2015 Sep;4(3):144-53. doi: 10.1055/s-0035-1564441. Epub 2015 Nov 30.
5
Overgrowth Syndromes.过度生长综合征
J Pediatr Genet. 2015 Sep;4(3):136-43. doi: 10.1055/s-0035-1564440. Epub 2015 Sep 25.
6
Somatic activating mutations in Pik3ca cause sporadic venous malformations in mice and humans.磷脂酰肌醇-3激酶催化亚基α(PIK3CA)的体细胞激活突变可导致小鼠和人类出现散发性静脉畸形。
Sci Transl Med. 2016 Mar 30;8(332):332ra43. doi: 10.1126/scitranslmed.aad9982.
7
Somatic PIK3CA mutations as a driver of sporadic venous malformations.体细胞PIK3CA突变作为散发性静脉畸形的驱动因素。
Sci Transl Med. 2016 Mar 30;8(332):332ra42. doi: 10.1126/scitranslmed.aaf1164.
8
mTORC1-mediated inhibition of polycystin-1 expression drives renal cyst formation in tuberous sclerosis complex.mTORC1介导的多囊蛋白-1表达抑制驱动结节性硬化症中的肾囊肿形成。
Nat Commun. 2016 Mar 2;7:10786. doi: 10.1038/ncomms10786.
9
Inactivation of the Class II PI3K-C2β Potentiates Insulin Signaling and Sensitivity.II类PI3K-C2β的失活增强胰岛素信号传导和敏感性。
Cell Rep. 2015 Dec 1;13(9):1881-94. doi: 10.1016/j.celrep.2015.10.052. Epub 2015 Nov 19.
10
How PI3K-derived lipids control cell division.磷脂酰肌醇-3激酶衍生的脂质如何控制细胞分裂。
Front Cell Dev Biol. 2015 Sep 30;3:61. doi: 10.3389/fcell.2015.00061. eCollection 2015.

组织过度增殖中的PI3K信号传导:从过度生长综合征到肾囊肿

PI3K Signaling in Tissue Hyper-Proliferation: From Overgrowth Syndromes to Kidney Cysts.

作者信息

De Santis Maria Chiara, Sala Valentina, Martini Miriam, Ferrero Giovanni Battista, Hirsch Emilio

机构信息

Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino 10126, Italy.

Department of Public Health and Pediatrics, University of Torino, Torino 10126, Italy.

出版信息

Cancers (Basel). 2017 Mar 29;9(4):30. doi: 10.3390/cancers9040030.

DOI:10.3390/cancers9040030
PMID:28353628
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5406705/
Abstract

The members of the PhosphoInositide-3 Kinase (PI3K) protein family are well-known regulators of proliferative signals. By the generation of lipid second messengers, they mediate the activation of AKT/PKB (AKT) and mammalian Target Of Rapamycin (mTOR) pathways. Although mutations in the PI3K/AKT/mTOR pathway are highly characterized in cancer, recent evidence indicates that alterations in the proliferative signals are major drivers of other diseases such as overgrowth disorders and polycystic kidney disease. In this review, we briefly summarize the role of the PI3K/AKT/mTOR pathway in cell proliferation by comparing the effect of alterations in PI3K enzymes in different tissues. In particular, we discuss the most recent findings on how the same pathway may lead to different biological effects, due to the convergence and cooperation of different signaling cascades.

摘要

磷酸肌醇-3激酶(PI3K)蛋白家族成员是众所周知的增殖信号调节因子。通过生成脂质第二信使,它们介导AKT/蛋白激酶B(AKT)和哺乳动物雷帕霉素靶蛋白(mTOR)信号通路的激活。尽管PI3K/AKT/mTOR信号通路中的突变在癌症中具有高度特征性,但最近的证据表明,增殖信号的改变是其他疾病(如过度生长障碍和多囊肾病)的主要驱动因素。在本综述中,我们通过比较不同组织中PI3K酶改变的影响,简要总结了PI3K/AKT/mTOR信号通路在细胞增殖中的作用。特别是,我们讨论了由于不同信号级联的汇聚和协作,同一信号通路如何导致不同生物学效应的最新发现。