Titlebook: Cellular Ageing and Replicative Senescence; Suresh I.S. Rattan,Leonard Hayflick Book 2016 The Editor(s) (if applicable) and The Author(s),

Addendum

书目名称Cellular Ageing and Replicative Senescence影响因子(影响力)




书目名称Cellular Ageing and Replicative Senescence影响因子(影响力)学科排名




书目名称Cellular Ageing and Replicative Senescence网络公开度




书目名称Cellular Ageing and Replicative Senescence网络公开度学科排名




书目名称Cellular Ageing and Replicative Senescence被引频次




书目名称Cellular Ageing and Replicative Senescence被引频次学科排名




书目名称Cellular Ageing and Replicative Senescence年度引用




书目名称Cellular Ageing and Replicative Senescence年度引用学科排名




书目名称Cellular Ageing and Replicative Senescence读者反馈




书目名称Cellular Ageing and Replicative Senescence读者反馈学科排名

可忽略

Influence of Donor Age and Species Longevity on Replicative Cellular Senescence when strains are obtained from different individuals. This variability is probably due to both technical issues and heterogeneity inside the tissues. Notwithstanding these limitations, many scientists searched for an inverse relationship of proliferative potential and donor age. Reviewing this lite

jarring

Ageing of the Stem Cells: The Conjoined Twosome Growing Old: Stem Cell and Its Nicheed, the stem cell and the niche are subject to aging. Potent mechanisms of biological aging are control of cellular metabolism, the action of aging genes, epigenetic drift and inflammation, which also modulate the cellular age of stem cells. A common feature of aged stem cells is however hyperactiva

GLOSS

Colonoscopy

善辩

Modeling Cellular Aging: An Introduction – Mathematical and Computational Approachesing. We find that there are a large array of methods from discrete to continuous and from deterministic to stochastic. This chapter is not meant to be a comprehensive coverage of all of the modeling efforts but rather a buffet introduction to what has been done in the field over the last 50–60 years

善辩

Cell Cycle Checkpoints and Senescenceageing studies. In a sharp contrast to cancer cells, it is firmly regulated by cell cycle checkpoints that ensure evasion of stressed and genetically modified cells, limiting their expansion and serve as an innate check to carcinogenesis. Tumour suppressors and their regulatory proteins play key rol

Cumulus

Mitochondrial Reactive Oxygen Species in Cellular SenescenceMitochondrial dysfunction is the principle cause of increased levels of reactive oxygen species (ROS) and oxidative stress, which is a key mediator of aging. The cell responds to this stressful stimulus by the induction of the cellular aging-stress response, cellular senescence. Here, we discuss the

APEX

Cellular Aging and Tumor Regulationcell, senescence can be one driving force of such diseases. In contrast, cancer is, on the one hand, associated with age as well, but can be seen as a gain of function disease. Cellular senescence can act to prevent cell proliferation and is believed to inhibit cancer growth. Interestingly, this tum

抱狗不敢前