The Role of Notch3 Signaling in Kidney Disease
Notch receptors are transmembrane proteins that are members of the epidermal growth factor-like family. These receptors are widely expressed on the cell surface and are highly conserved. Binding to ligands on adjacent cells results in cleavage of these receptors, and their intracellular domains tran...
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Series: | Oxidative Medicine and Cellular Longevity |
Online Access: | http://dx.doi.org/10.1155/2020/1809408 |
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doaj-ecf4a4575bb544afaead18efaf916cda2020-11-25T03:04:32ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942020-01-01202010.1155/2020/18094081809408The Role of Notch3 Signaling in Kidney DiseaseCheng Yuan0Lihua Ni1Changjiang Zhang2Xiaoyan Wu3Department of Gynecological Oncology, Zhongnan Hospital of Wuhan University, Wuhan 430071, ChinaDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan 430071, ChinaDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, ChinaDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan 430071, ChinaNotch receptors are transmembrane proteins that are members of the epidermal growth factor-like family. These receptors are widely expressed on the cell surface and are highly conserved. Binding to ligands on adjacent cells results in cleavage of these receptors, and their intracellular domains translocate into the nucleus, where target gene transcription is initiated. In the mammalian kidney, Notch receptors are activated during nephrogenesis and become silenced in the normal kidney after birth. Reactivation of Notch signaling in the adult kidney could be due to the genetic activation of Notch signaling or kidney injury. Notch3 is a mammalian heterodimeric transmembrane receptor in the Notch gene family. Notch3 activation is significantly increased in various glomerular diseases, renal tubulointerstitial diseases, glomerular sclerosis, and renal fibrosis and mediates disease occurrence and development. Here, we discuss numerous recently published papers describing the role of Notch3 signaling in kidney disease.http://dx.doi.org/10.1155/2020/1809408 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Cheng Yuan Lihua Ni Changjiang Zhang Xiaoyan Wu |
spellingShingle |
Cheng Yuan Lihua Ni Changjiang Zhang Xiaoyan Wu The Role of Notch3 Signaling in Kidney Disease Oxidative Medicine and Cellular Longevity |
author_facet |
Cheng Yuan Lihua Ni Changjiang Zhang Xiaoyan Wu |
author_sort |
Cheng Yuan |
title |
The Role of Notch3 Signaling in Kidney Disease |
title_short |
The Role of Notch3 Signaling in Kidney Disease |
title_full |
The Role of Notch3 Signaling in Kidney Disease |
title_fullStr |
The Role of Notch3 Signaling in Kidney Disease |
title_full_unstemmed |
The Role of Notch3 Signaling in Kidney Disease |
title_sort |
role of notch3 signaling in kidney disease |
publisher |
Hindawi Limited |
series |
Oxidative Medicine and Cellular Longevity |
issn |
1942-0900 1942-0994 |
publishDate |
2020-01-01 |
description |
Notch receptors are transmembrane proteins that are members of the epidermal growth factor-like family. These receptors are widely expressed on the cell surface and are highly conserved. Binding to ligands on adjacent cells results in cleavage of these receptors, and their intracellular domains translocate into the nucleus, where target gene transcription is initiated. In the mammalian kidney, Notch receptors are activated during nephrogenesis and become silenced in the normal kidney after birth. Reactivation of Notch signaling in the adult kidney could be due to the genetic activation of Notch signaling or kidney injury. Notch3 is a mammalian heterodimeric transmembrane receptor in the Notch gene family. Notch3 activation is significantly increased in various glomerular diseases, renal tubulointerstitial diseases, glomerular sclerosis, and renal fibrosis and mediates disease occurrence and development. Here, we discuss numerous recently published papers describing the role of Notch3 signaling in kidney disease. |
url |
http://dx.doi.org/10.1155/2020/1809408 |
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