ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.
about
Hydrogen Peroxide and Sodium Transport in the Lung and KidneyROS and ROS-Mediated Cellular SignalingChronic Ethanol Exposure: Pathogenesis of Pulmonary Disease and DysfunctionInhibition of ENaC by endothelin-1Role of Rho GDP dissociation inhibitor α in control of epithelial sodium channel (ENaC)-mediated sodium reabsorptionIGF-1 and insulin exert opposite actions on ClC-K2 activity in the cortical collecting ductsReactive oxygen species as important determinants of medullary flow, sodium excretion, and hypertensionH-Ras mediates the inhibitory effect of epidermal growth factor on the epithelial Na+ channelCross-talk between insulin and IGF-1 receptors in the cortical collecting duct principal cells: implication for ENaC-mediated Na+ reabsorption.Endothelial Mineralocorticoid Receptor Mediates Diet-Induced Aortic Stiffness in FemalesInsulin and IGF-1 activate Kir4.1/5.1 channels in cortical collecting duct principal cells to control basolateral membrane voltage.Regulation of ENaC in mice lacking renal insulin receptors in the collecting duct.Deficiency of renal cortical EGF increases ENaC activity and contributes to salt-sensitive hypertension.Toll-like receptor 7 affects the pathogenesis of non-alcoholic fatty liver disease.Epidermal growth factors in the kidney and relationship to hypertension.Activation of ENaC in collecting duct cells by prorenin and its receptor PRR: involvement of Nox4-derived hydrogen peroxidePhosphatase and tensin homolog deleted on chromosome 10 (PTEN) signaling regulates mitochondrial biogenesis and respiration via estrogen-related receptor α (ERRα).Formaldehyde impairs transepithelial sodium transport.Pro-survival redox signalling in progesterone-mediated retinal neuroprotection.Involvement of ENaC in the development of salt-sensitive hypertension.Oxidative Stress and Hypertensive Diseases.Fulvene-5 inhibition of Nadph oxidases attenuates activation of epithelial sodium channels in A6 distal nephron cells.The Epigenetic Machinery in Vascular Dysfunction and Hypertension.Novel mechanisms for crotonaldehyde-induced lung edema.
P2860
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P2860
ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
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2012年论文
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name
ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.
@ast
ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.
@en
type
label
ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.
@ast
ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.
@en
prefLabel
ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.
@ast
ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.
@en
P2093
P2860
P1476
ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1
@en
P2093
Daria V Ilatovskaya
Tengis S Pavlov
Vladislav Levchenko
P2860
P304
P356
10.1152/AJPCELL.00231.2012
P577
2012-11-07T00:00:00Z