Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
J Mol Neurosci. 2011 Nov;45(3):445-52. doi: 10.1007/s12031-011-9588-1. Epub 2011 Jul 5.
The c-Abl tyrosine kinase participates in a variety of cellular functions, including regulation of the actin cytoskeleton, regulation of the cell cycle, and the apoptotic/cell cycle arrest response to stress, and the Abl family of kinases has been shown to play a crucial role in development of the central nervous system. Recent studies have shown c-Abl activation in human Alzheimer's and Parkinson's diseases and c-Abl activation in mouse models and neuronal culture in response to amyloid beta fibrils and oxidative stress. Overexpression of active c-Abl in adult mouse neurons results in neurodegeneration and neuroinflammation. Based on this evidence, a potential role for c-Abl in the pathogenesis of neurodegenerative disease is discussed, and we attempt to place activation of c-Abl in context with other known contributors to neurodegenerative pathology.
c-Abl 酪氨酸激酶参与多种细胞功能,包括肌动蛋白细胞骨架的调节、细胞周期的调节以及应激诱导的细胞凋亡/细胞周期阻滞反应,Abl 激酶家族已被证明在中枢神经系统的发育中起着至关重要的作用。最近的研究表明,c-Abl 在人类阿尔茨海默病和帕金森病中的激活,以及 c-Abl 在小鼠模型和神经元培养中对淀粉样β纤维和氧化应激的反应中的激活。在成年小鼠神经元中过表达活性 c-Abl 会导致神经退行性变和神经炎症。基于这些证据,讨论了 c-Abl 在神经退行性疾病发病机制中的潜在作用,我们试图将 c-Abl 的激活与其他已知的神经退行性病理贡献因素联系起来。