Impairment of lon-induced protection against the accumulation of oxidized proteins in senescent wi-38 fibroblasts
about
Mitochondrial Lon protease in human disease and aging: Including an etiologic classification of Lon-related diseases and disordersOxygen consumption and usage during physical exercise: the balance between oxidative stress and ROS-dependent adaptive signalingInhibition of Lon protease by triterpenoids alters mitochondria and is associated to cell death in human cancer cells.The age- and sex-specific decline of the 20s proteasome and the Nrf2/CncC signal transduction pathway in adaption and resistance to oxidative stress in Drosophila melanogasterDopamine quinone modifies and decreases the abundance of the mitochondrial selenoprotein glutathione peroxidase 4.On the Relationship between Energy Metabolism, Proteostasis, Aging and Parkinson's Disease: Possible Causative Role of Methylglyoxal and Alleviative Potential of Carnosine.Upregulation of the mitochondrial Lon Protease allows adaptation to acute oxidative stress but dysregulation is associated with chronic stress, disease, and aging.Distinct quaternary structures of the AAA+ Lon protease control substrate degradation.Inhibition of Lon blocks cell proliferation, enhances chemosensitivity by promoting apoptosis and decreases cellular bioenergetics of bladder cancer: potential roles of Lon as a prognostic marker and therapeutic target in baldder cancer.Substrate- and isoform-specific proteome stability in normal and stressed cardiac mitochondriaSpatial and temporal dynamics of the cardiac mitochondrial proteome.The peroxisomal Lon protease LonP2 in aging and disease: functions and comparisons with mitochondrial Lon protease LonP1The decay of Redox-stress Response Capacity is a substantive characteristic of aging: Revising the redox theory of aging.Sexual Dimorphism and Aging Differentially Regulate Adaptive Homeostasis.The Proteasome and Oxidative Stress in Alzheimer's Disease.Differential roles of proteasome and immunoproteasome regulators Pa28αβ, Pa28γ and Pa200 in the degradation of oxidized proteins.NaDC3 Induces Premature Cellular Senescence by Promoting Transport of Krebs Cycle Intermediates, Increasing NADH, and Exacerbating Oxidative Damage.The Mitochondrial Lon Protease Is Required for Age-Specific and Sex-Specific Adaptation to Oxidative Stress.Redox Regulation of Homeostasis and Proteostasis in Peroxisomes.The role of declining adaptive homeostasis in ageing.The mitochondrial unfolded protein response and mitohormesis: a perspective on metabolic diseases
P2860
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P2860
Impairment of lon-induced protection against the accumulation of oxidized proteins in senescent wi-38 fibroblasts
description
2011 nî lūn-bûn
@nan
2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Impairment of lon-induced prot ...... in senescent wi-38 fibroblasts
@ast
Impairment of lon-induced prot ...... in senescent wi-38 fibroblasts
@en
type
label
Impairment of lon-induced prot ...... in senescent wi-38 fibroblasts
@ast
Impairment of lon-induced prot ...... in senescent wi-38 fibroblasts
@en
prefLabel
Impairment of lon-induced prot ...... in senescent wi-38 fibroblasts
@ast
Impairment of lon-induced prot ...... in senescent wi-38 fibroblasts
@en
P2093
P2860
P356
P1476
Impairment of lon-induced prot ...... in senescent wi-38 fibroblasts
@en
P2093
Alison L Koop
Daniela A Bota
Jenny K Ngo
Kelvin J A Davies
Laura C D Pomatto
P2860
P304
P356
10.1093/GERONA/GLR145
P407
P577
2011-08-24T00:00:00Z