磷酸化
安普克
激酶
细胞生物学
微管
化学
蛋白质磷酸化
蛋白激酶A
τ蛋白
微管相关蛋白
丝氨酸苏氨酸激酶
AMP活化蛋白激酶
生物
医学
内科学
阿尔茨海默病
疾病
作者
Hirotaka Yoshida,Michel Goedert
标识
DOI:10.1111/j.1471-4159.2011.07523.x
摘要
J. Neurochem. (2012) 120 , 165–176. Abstract Microtubule‐associated protein tau is abnormally hyperphosphorylated in the intracellular filamentous inclusions seen in neurodegenerative disorders with dementia, such as Alzheimer’s disease and other tauopathies. Microtubule‐associated protein/microtubule‐affinity regulating kinases (MARKs) have previously been identified as kinases which phosphorylate KxGS motifs in the tandem repeats of tau. They are members of the 5′‐AMP‐activated protein kinase (AMPK)‐related kinases in the Ca 2+ /calmodulin‐dependent protein kinase group. In this study, we examined the ability of AMPK‐related kinases, brain‐specific kinases 1 and 2, maternal embryonic leucine‐zipper kinase, MARK1, and salt‐inducible kinase (SIK), to phosphorylate tau. We found that they phosphorylated S262 and S356 in KxGS motifs in the repeats of tau, thus resulting in immunoreactivity with antibody 12E8. MARK1 and SIK most effectively phosphorylated tau, and their down‐regulation resulted in a reduction of 12E8‐labelling. BX 795, an inhibitor of MARK1 and SIK, reduced 12E8‐immunolabelling of tau in rat cortical neurons. These findings reveal a significant contribution of AMPK‐related kinases to the phosphorylation of tau at S262/S356.
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