Fibroblasts from long-lived mutant mice exhibit increased autophagy and lower TOR activity after nutrient deprivation or oxidative stress.
about
Rapalogs and mTOR inhibitors as anti-aging therapeuticsBig mice die young but large animals live longerFibroblasts derived from long-lived insulin receptor substrate 1 null mice are not resistant to multiple forms of stress.Elevated ATF4 function in fibroblasts and liver of slow-aging mutant mice.Far-infrared suppresses skin photoaging in ultraviolet B-exposed fibroblasts and hairless miceHypothalamic-Pituitary Axis Regulates Hydrogen Sulfide Production.Reduced in vivo hepatic proteome replacement rates but not cell proliferation rates predict maximum lifespan extension in mice.Recent discoveries in the cycling, growing and aging of the p53 fieldThe Somatotropic Axis in Human Aging: Framework for the Current State of Knowledge and Future ResearchMTOR-driven quasi-programmed aging as a disposable soma theory: blind watchmaker vs. intelligent designer.M(o)TOR of aging: MTOR as a universal molecular hypothalamusImpaired autophagy activity is linked to elevated ER-stress and inflammation in aging adipose tissueAging is not programmed: genetic pseudo-program is a shadow of developmental growth.Liver-specific GH receptor gene-disrupted (LiGHRKO) mice have decreased endocrine IGF-I, increased local IGF-I, and altered body size, body composition, and adipokine profilesP62/SQSTM1 at the interface of aging, autophagy, and disease.M(o)TOR of pseudo-hypoxic state in aging: rapamycin to the rescue.IGF-1 deficiency in a critical period early in life influences the vascular aging phenotype in mice by altering miRNA-mediated post-transcriptional gene regulation: implications for the developmental origins of health and disease hypothesis.Dramatic antitumor effects of the dual mTORC1 and mTORC2 inhibitor AZD2014 in hepatocellular carcinoma.Gasotransmitter hydrogen sulfide signaling in neuronal health and disease.
P2860
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P2860
Fibroblasts from long-lived mutant mice exhibit increased autophagy and lower TOR activity after nutrient deprivation or oxidative stress.
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
@zh
2012年论文
@zh-cn
name
Fibroblasts from long-lived mu ...... privation or oxidative stress.
@ast
Fibroblasts from long-lived mu ...... privation or oxidative stress.
@en
type
label
Fibroblasts from long-lived mu ...... privation or oxidative stress.
@ast
Fibroblasts from long-lived mu ...... privation or oxidative stress.
@en
prefLabel
Fibroblasts from long-lived mu ...... privation or oxidative stress.
@ast
Fibroblasts from long-lived mu ...... privation or oxidative stress.
@en
P2860
P1433
P1476
Fibroblasts from long-lived mu ...... privation or oxidative stress.
@en
P2093
Richard A Miller
P2860
P304
P356
10.1111/J.1474-9726.2012.00833.X
P577
2012-06-04T00:00:00Z