Apoptosis, proliferation, differentiation: in search of the order
Apoptosis, proliferation, differentiation: in search of the order
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DOI：
10.1016/s1044-579x(02)00127-x
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发表时间：
2003-04-01
影响因子：
14.5
通讯作者：
Blagosklonny, MV
中科院分区：
文献类型：
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作者：
Blagosklonny, MV
在寻找这个顺序的过程中，我们试图将细胞死亡、增殖、分化和衰老普遍联系起来。当前的模型（经典的、相互冲突的信号和定量信号模型）受到限制，正是因为它们试图对细胞反应的过多终点进行hardware，通过在分子术语中定义每个细胞过程，可以断开增殖（CDK激活）、凋亡（caspase激活）和分化（组织功能基因表达），即使这些反应是通过上游信号转导途径联系在一起的。这些矛盾的途径（如有丝分裂原激活的途径）同时转导相反的信号（用于生长停止和循环，用于细胞死亡和存活），这些信号最终被翻译成所有可能的细胞反应组合。当在多维轴上描述时，这个通用模型也可能包括侵袭性、衰老、转移性和血管生成反应，甚至包括恶性转化等整体特征。2003爱思唯尔科学有限公司版权所有。
In search of the order, we are tempted to universally link cell death, proliferation, differentiation, and senescence. Current models (classical, conflicting signal and quantitative signal models) are restricted, precisely because they attempt to hardware a plethora of end-points of cellular responses, By defining each cellular process in, molecular term, one can disconnect proliferation (CDK activation), apoptosis (caspase activation), and differentiation (tissue function genes expression), even though these responses are linked by upstream signal transduction pathways. These ambivalent pathways (e.g. mitogen-activated pathways) simultaneously transduce opposite signals (for growth arrest and cycling, for cell death and survival), which are ultimately translated in all possible combinations of cellular responses. When depicted in multidimensional axis, this universal model may also include invasiveness, senescence, metastatic and angiogenic responses and even such integral characteristics as malignant transformation. (C) 2003 Elsevier Science Ltd. All rights reserved.