Program-like aging and mitochondria: instead of random damage by free radicals.
about
Testing predictions of the programmed and stochastic theories of aging: comparison of variation in age at death, menopause, and sexual maturationWhy men age faster but reproduce longer than women: mTOR and evolutionary perspectivesIn search of antiaging modalities: evaluation of mTOR- and ROS/DNA damage-signaling by cytometry.Why the disposable soma theory cannot explain why women live longer and why we age.Potential anti-aging agents suppress the level of constitutive mTOR- and DNA damage- signalingAged iPSCs display an uncommon mitochondrial appearance and fail to undergo in vitro neurogenesis.Hormesis does not make sense except in the light of TOR-driven aging.Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR inhibitors: rationale and importance to inhibiting these pathways in human health.Molecular damage in cancer: an argument for mTOR-driven agingIs cancer a metabolic rebellion against host aging? In the quest for immortality, tumor cells try to save themselves by boosting mitochondrial metabolismLithocholic acid extends longevity of chronologically aging yeast only if added at certain critical periods of their lifespan.Answering the ultimate question "what is the proximal cause of aging?"Detoxification reactions: relevance to aging.Dominant roles of the Raf/MEK/ERK pathway in cell cycle progression, prevention of apoptosis and sensitivity to chemotherapeutic drugs.The Raf/MEK/ERK pathway can govern drug resistance, apoptosis and sensitivity to targeted therapy.Enhancing therapeutic efficacy by targeting non-oncogene addicted cells with combinations of signal transduction inhibitors and chemotherapyAging is not programmed: genetic pseudo-program is a shadow of developmental growth.Emerging MEK inhibitors.Genome-wide RNA-seq of iPSC-derived motor neurons indicates selective cytoskeletal perturbation in Brown-Vialetto disease that is partially rescued by riboflavin.Current status of auditory aging and anti-aging research.Impairment of regeneration in aging: appropriateness or stochastics?What is the Proximal Cause of Aging?Endonuclease G promotes mitochondrial genome cleavage and replication.Spontaneous mutations in CYC8 and MIG1 suppress the short chronological lifespan of budding yeast lacking SNF1/AMPK.
P2860
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P2860
Program-like aging and mitochondria: instead of random damage by free radicals.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Program-like aging and mitochondria: instead of random damage by free radicals.
@en
type
label
Program-like aging and mitochondria: instead of random damage by free radicals.
@en
prefLabel
Program-like aging and mitochondria: instead of random damage by free radicals.
@en
P2860
P356
P1476
Program-like aging and mitochondria: instead of random damage by free radicals.
@en
P2860
P304
P356
10.1002/JCB.21602
P577
2007-12-01T00:00:00Z