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The Mechanism of Kidney Disease Due to APOL1 Risk Variants.

作者信息

Pays Etienne

机构信息

Laboratory of Molecular Parasitology, IBMM, Université Libre de Bruxelles, Gosselies, Belgium

出版信息

J Am Soc Nephrol. 2020 Nov;31(11):2502-2505. doi: 10.1681/ASN.2020070954. Epub 2020 Sep 17.

Abstract
摘要

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本文引用的文献

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Kidney-Risk Variants Induce Mitochondrial Fission.
Kidney Int Rep. 2020 Mar 30;5(6):891-904. doi: 10.1016/j.ekir.2020.03.020. eCollection 2020 Jun.
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Golgi-derived PI4P-containing vesicles drive late steps of mitochondrial division.
Science. 2020 Mar 20;367(6484):1366-1371. doi: 10.1126/science.aax6089.
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APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin.
Cell Rep. 2020 Mar 17;30(11):3821-3836.e13. doi: 10.1016/j.celrep.2020.02.064.
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and Kidney Disease: From Genetics to Biology.
Annu Rev Physiol. 2020 Feb 10;82:323-342. doi: 10.1146/annurev-physiol-021119-034345. Epub 2019 Nov 11.
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ATG9A shapes the forming autophagosome through Arfaptin 2 and phosphatidylinositol 4-kinase IIIβ.
J Cell Biol. 2019 May 6;218(5):1634-1652. doi: 10.1083/jcb.201901115. Epub 2019 Mar 27.

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