نتایج جستجو برای: polyploidy

تعداد نتایج: 3304  

2013
Ling-Ling Liu Zi-Jie Long Le-Xun Wang Fei-Meng Zheng Zhi-Gang Fang Min Yan Dong-Fan Xu Jia-Jie Chen Shao-Wu Wang Dong-Jun Lin Quentin Liu

Aurora kinases are overexpressed in large numbers of tumors and considered as potential therapeutic targets. In this study, we found that the Aurora kinases inhibitors MK-0457 (MK) and ZM447439 (ZM) induced polyploidization in acute myeloid leukemia (AML) cell lines. The level of glycolytic metabolism was significantly increased in the polyploidy cells, which were sensitive to glycolysis inhibi...

Journal: :Journal of General Physiology 1950

Journal: :British Journal of Cancer 1978

Journal: :Evolution 1973

Journal: :Circulation research 2010
Zhipei Liu Shijing Yue Xiaobo Chen Thomas Kubin Thomas Braun

RATIONALE Polyploidy and multinucleation are characteristic features of mammalian cardiomyocytes, which develop shortly after birth when most differentiated cardiomyocytes become acytokinetic. Cardiac overload and hypertrophy further increase the degree of polyploidy of cardiomyocytes, suggesting a role in cell type-specific responses to physiological and pathological stimuli. OBJECTIVE We so...

2010

Liu et al have discovered a potent promoter of polyploidy in rat hearts. Polyploidy—multiple copies of the genome in one cell—is normal in cardiomyocytes but can also be ramped up in pathological situations, such as cardiac hypertrophy or in regenerative situations, such as after heart injury. The ability to boost or suppress polyploidy might thus have a number of heart health implications. Car...

2004
A. R. Leitch D. E. Soltis P. S. Soltis I. J. Leitch J. C. Pires B. K. MABLE

Although polyploidy has been involved in speciation in both animals and plants, the general perception is often that it is too rare to have been a significant factor in animal evolution and its role in plant diversification has been questioned. These views have resulted in a bias towards explanations for what deters polyploidy, rather than the somewhat more interesting question of the mechanism...

2016
Akihiro Ohashi

The molecular mechanism responsible for cell fate after mitotic slippage remains unclear. We investigated the different postmitotic effects of aneuploidy versus polyploidy using chemical inhibitors of centromere-associated protein-E (CENP-E) and kinesin family member 11 (KIF11, also known as Eg5). Aneuploidy caused substantial proteotoxic stress and DNA damage accompanied by p53-mediated postmi...

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