The Role of c-Abl Tyrosine Kinase in Brain and Its Pathologies

被引:9
作者
Motaln, Helena [1 ]
Rogelj, Boris [1 ,2 ]
机构
[1] Jozef Stefan Inst, Dept Biotechnol, Ljubljana 1000, Slovenia
[2] Univ Ljubljana, Fac Chem & Chem Technol, Ljubljana 1000, Slovenia
关键词
c-Abl (Abelson) tyrosine kinase; neurodegeneration; Alzheimer's disease; Parkinson's disease; kinase signaling; IMPROVES NEUROLOGICAL SYMPTOMS; AMYLOID-BETA OLIGOMERS; ALPHA-SYNUCLEIN; NEURONAL MIGRATION; INDUCED APOPTOSIS; MOUSE MODEL; PHOSPHORYLATION; PROTEIN; ACTIVATION; TAU;
D O I
10.3390/cells12162041
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Differentiated status, low regenerative capacity and complex signaling make neuronal tissues highly susceptible to translating an imbalance in cell homeostasis into cell death. The high rate of neurodegenerative diseases in the elderly population confirms this. The multiple and divergent signaling cascades downstream of the various stress triggers challenge researchers to identify the central components of the stress-induced signaling pathways that cause neurodegeneration. Because of their critical role in cell homeostasis, kinases have emerged as one of the key regulators. Among kinases, non-receptor tyrosine kinase (Abelson kinase) c-Abl appears to be involved in both the normal development of neural tissue and the development of neurodegenerative pathologies when abnormally expressed or activated. However, exactly how c-Abl mediates the progression of neurodegeneration remains largely unexplored. Here, we summarize recent findings on the involvement of c-Abl in normal and abnormal processes in nervous tissue, focusing on neurons, astrocytes and microglial cells, with particular reference to molecular events at the interface between stress signaling, DNA damage, and metabolic regulation. Because inhibition of c-Abl has neuroprotective effects and can prevent neuronal death, we believe that an integrated view of c-Abl signaling in neurodegeneration could lead to significantly improved treatment of the disease.
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页数:23
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