MAPK/ERK通路
蛋白激酶A
信号转导
激酶
细胞生物学
p38丝裂原活化蛋白激酶
发病机制
生物
丝裂原活化蛋白激酶
磷酸化
丝裂原活化蛋白激酶3
免疫学
作者
Xiongwei Zhu,Hyoung‐gon Lee,Arun K. Raina,George Perry,Mark A. Smith
出处
期刊:Neurosignals
[Cell Physiol Biochem Press GmbH and Co KG]
日期:2002-01-01
卷期号:11 (5): 270-281
被引量:371
摘要
Given the critical role of mitogen-activated protein kinase (MAPK) pathways in regulating cellular processes that are affected in Alzheimer's disease (AD), the importance of MAPKs in disease pathogenesis is being increasingly recognized. All MAPK pathways, i.e., the extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 pathways, are activated in vulnerable neurons in patients with AD suggesting that MAPK pathways are involved in the pathophysiology and pathogenesis of AD. Here we review recent findings implicating the MAPK pathways in AD and discuss the relationship between these pathways and the prominent pathological processes, i.e., tau phosphorylation and amyloid-β deposition, as well as the functional association to amyloid β protein precursor. We suggest that regulation of these pathways may be a central facet to any potential treatment for the disease.
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