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mTOR is out of control in polycystic kidney disease.在多囊肾病中,mTOR失去控制。
Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5247-8. doi: 10.1073/pnas.0601352103. Epub 2006 Mar 27.
2
Polycystic kidney disease.多囊肾病
N Engl J Med. 2004 Jan 8;350(2):151-64. doi: 10.1056/NEJMra022161.
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PKD: a progress report, new directions in research.多囊肾病:进展报告及研究新方向
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Polycystic kidney disease--a tale of calcium channels and the actin cytoskeleton.
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Polycystic kidney disease--what's new?多囊肾病——有什么新进展?
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[From gene to disease; from polycystines to polycystic kidney disease].从基因到疾病;从多囊蛋白到多囊肾病
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Identification and Characterization of Novel Mutations in Chronic Kidney Disease (CKD) and Autosomal Dominant Polycystic Kidney Disease (ADPKD) in Saudi Subjects by Whole-Exome Sequencing.通过全外显子组测序鉴定和分析沙特患者慢性肾脏病(CKD)和常染色体显性多囊肾病(ADPKD)中的新型突变。
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Loss of Fnip1 alters kidney developmental transcriptional program and synergizes with TSC1 loss to promote mTORC1 activation and renal cyst formation.FNIP1 的缺失改变了肾脏发育的转录程序,并与 TSC1 的缺失协同作用,促进 mTORC1 的激活和肾脏囊肿的形成。
PLoS One. 2018 Jun 13;13(6):e0197973. doi: 10.1371/journal.pone.0197973. eCollection 2018.
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Revealing protein networks and gene-drug connectivity in cancer from direct information.从直接信息中揭示癌症中的蛋白质网络和基因-药物关联。
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Congenital hepatic fibrosis in autosomal recessive polycystic kidney disease.常染色体隐性多囊肾病中的先天性肝纤维化。
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Loss of primary cilia upregulates renal hypertrophic signaling and promotes cystogenesis.原发性纤毛丧失会上调肾脏肥大信号通路并促进囊肿形成。
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Polycystic kidney disease: pathogenesis and potential therapies.多囊肾病:发病机制与潜在治疗方法
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The tuberous sclerosis proteins regulate formation of the primary cilium via a rapamycin-insensitive and polycystin 1-independent pathway.结节性硬化蛋白通过一种不依赖雷帕霉素且不依赖多囊蛋白1的途径调节初级纤毛的形成。
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10
Treatment of autosomal dominant polycystic kidney disease (ADPKD): the new horizon for children with ADPKD.常染色体显性多囊肾病(ADPKD)的治疗:ADPKD患儿的新视野。
Pediatr Nephrol. 2008 Jul;23(7):1029-36. doi: 10.1007/s00467-007-0706-9. Epub 2008 Feb 8.

本文引用的文献

1
The mTOR pathway is regulated by polycystin-1, and its inhibition reverses renal cystogenesis in polycystic kidney disease.mTOR信号通路受多囊蛋白-1调控,抑制该通路可逆转多囊肾病中的肾囊肿形成。
Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5466-71. doi: 10.1073/pnas.0509694103. Epub 2006 Mar 27.
2
Polycystin-1, STAT6, and P100 function in a pathway that transduces ciliary mechanosensation and is activated in polycystic kidney disease.多囊蛋白-1、信号转导和转录激活因子6(STAT6)以及P100在一条传导纤毛机械感觉并在多囊肾病中被激活的信号通路中发挥作用。
Dev Cell. 2006 Jan;10(1):57-69. doi: 10.1016/j.devcel.2005.12.005.
3
Rapamycin: an anti-cancer immunosuppressant?雷帕霉素:一种抗癌免疫抑制剂?
Crit Rev Oncol Hematol. 2005 Oct;56(1):47-60. doi: 10.1016/j.critrevonc.2004.09.009.
4
Dysregulation of the TSC-mTOR pathway in human disease.人类疾病中TSC-mTOR通路的失调。
Nat Genet. 2005 Jan;37(1):19-24. doi: 10.1038/ng1494.
5
Intraflagellar transport and cilia-dependent renal disease: the ciliary hypothesis of polycystic kidney disease.鞭毛内运输与纤毛相关的肾脏疾病:多囊肾病的纤毛假说
J Am Soc Nephrol. 2004 Oct;15(10):2528-36. doi: 10.1097/01.ASN.0000141055.57643.E0.
6
Cystic kidney diseases: all roads lead to the cilium.
Physiology (Bethesda). 2004 Aug;19:225-30. doi: 10.1152/physiol.00003.2004.
7
TSC2: filling the GAP in the mTOR signaling pathway.结节性硬化症复合物2(TSC2):填补mTOR信号通路中的空白
Trends Biochem Sci. 2004 Jan;29(1):32-8. doi: 10.1016/j.tibs.2003.11.007.
8
Autosomal dominant polycystic kidney disease.常染色体显性多囊肾病
Nefrologia. 2003;23 Suppl 1:14-22.
9
Autosomal dominant polycystic kidney disease: molecular genetics and pathophysiology.常染色体显性多囊肾病:分子遗传学与病理生理学
J Lab Clin Med. 2003 Feb;141(2):91-101. doi: 10.1067/mlc.2003.13.
10
Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells.多囊蛋白1和2介导肾细胞初级纤毛中的机械感觉。
Nat Genet. 2003 Feb;33(2):129-37. doi: 10.1038/ng1076. Epub 2003 Jan 6.

mTOR is out of control in polycystic kidney disease.

作者信息

Mostov Keith E

机构信息

Department of Anatomy, School of Medicine, University of California-San Francisco, Genentech Hall Room N212B, Box 2140, 600 16th Street, San Francisco, CA 94147, USA.

出版信息

Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5247-8. doi: 10.1073/pnas.0601352103. Epub 2006 Mar 27.

DOI:10.1073/pnas.0601352103
PMID:16567652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1459339/
Abstract
摘要