内质网和视角

描述

细胞凋亡可能是一种程序化的渐进性坏死,发生在细胞生物。有机化学事件导致细胞变化特征(形态)和死亡。这些变化拥抱起泡,细胞收缩,核分裂,身体物质冷凝,身体聚合物碎片,globalm RNA衰变。典型的成年人失去每天50至七百亿细胞因为caspase-mediated细胞死亡。人类平均8到14岁之间的孩子,每天大约20 - 30美元细胞死亡。脱疽的区别,这可能是一种创伤性渐进性坏死所导致的急性细胞损伤,caspase-mediated细胞死亡可能是一个非常规范的相关控制方法,有利于整个生物体的生命周期。例如,手指和脚趾的分离非常发展中人类胚胎发生的细胞之间的数字熊caspase-mediated细胞死亡。不喜欢脱疽,caspase-mediated细胞死亡所产生的细胞碎片被称为凋亡的身体,营养细胞准备吞噬并带走细胞将波及到的内容之前关闭细胞,造成伤害。因为caspase-mediated细胞死亡不能阻止一旦它开始,它是一个非常规范的方法。Caspase-mediated细胞死亡通路之间的开始通常是通过一个2。 Within the intrinsic pathway the cell kills itself as a result of it senses cell stress, whereas within the accidental pathway the cell kills itself as a result of signals from alternative cells. Weak external signals may activate the intrinsic pathway of caspase-mediated cell death. Each pathway induces necrobiosis by activating caspases, that are proteases, or enzymes that degrade proteins. The 2 pathways each activate leader caspases that then activate public executioner caspases that then kill the cell by degrading proteins indiscriminately. In addition to its importance as a biological development, defective apoptotic processes are concerned in a very big variety of diseases. Excessive caspase-mediated cell death causes atrophy, whereas associate scant quantity leads to uncontrolled cell proliferation, like cancer. Some factors like Fas receptors and caspases promote caspase-mediated cell death, whereas some members of the Bcl-2 family of proteins inhibit caspase-mediated cell death. The initiation of caspase-mediated cell death is tightly regulated by activation mechanisms, as a result of once caspase-mediated cell death has begun; it inevitably results in the death of the cell. The 2 best-understood activation mechanisms are the intrinsic pathway (also referred to as the mitochondrial pathway) and therefore the accidental pathway. The intrinsic pathway is activated by living thing signals generated once cells are stressed and depends on the discharge of proteins from the intermembrane house of mitochondria.The accidental pathway is activated by living thing ligands binding to cell-surface death receptors, that results in the formation of the death-inducing sign complicated (DISC). A cell inductees living thing apoptotic sign in response to a stress, which can bring forth, cell suicide. The required of nuclear receptors by glucocorticoids, heat, radiation, nutrient deprivation, virus infection, hypoxia, inflated living thing concentration of free fatty acids and inflated living thing CA concentration, for instance, by harm to the membrane, will all trigger the discharge of living thing apoptotic signals by a broken cell. Variety of cellular parts, like poly ADP saccharide enzyme, may facilitate regulate caspase-mediated cell death. Single cell fluctuations are discovered in experimental studies of stress elicited caspase-mediated cell death.