Manzoni Claudia, Mamais Adamantios, Roosen Dorien A, Dihanich Sybille, Soutar Marc P M, Plun-Favreau Helene, Bandopadhyay Rina, Hardy John, Tooze Sharon A, Cookson Mark R, Lewis Patrick A
School of Pharmacy, University of Reading, Whiteknights, Reading, RG6 6AP, United Kingdom.
Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom.
Sci Rep. 2016 Oct 12;6:35106. doi: 10.1038/srep35106.
Leucine rich repeat kinase 2 is a complex enzyme with both kinase and GTPase activities, closely linked to the pathogenesis of several human disorders including Parkinson's disease, Crohn's disease, leprosy and cancer. LRRK2 has been implicated in numerous cellular processes; however its physiological function remains unclear. Recent reports suggest that LRRK2 can act to regulate the cellular catabolic process of macroautophagy, although the precise mechanism whereby this occurs has not been identified. To investigate the signalling events through which LRRK2 acts to influence macroautophagy, the mammalian target of rapamycin (mTOR)/Unc-51-like kinase 1 (ULK1) and Beclin-1/phosphatidylinositol 3-kinase (PI3K) pathways were evaluated in astrocytic cell models in the presence and absence of LRRK2 kinase inhibitors. Chemical inhibition of LRRK2 kinase activity resulted in the stimulation of macroautophagy in a non-canonical fashion, independent of mTOR and ULK1, but dependent upon the activation of Beclin 1-containing class III PI3-kinase.
富含亮氨酸重复激酶2是一种具有激酶和GTP酶活性的复合酶,与包括帕金森病、克罗恩病、麻风病和癌症在内的多种人类疾病的发病机制密切相关。LRRK2参与了众多细胞过程;然而其生理功能仍不清楚。最近的报告表明,LRRK2可调节巨自噬的细胞分解代谢过程,尽管其发生的确切机制尚未明确。为了研究LRRK2影响巨自噬的信号转导事件,在有和没有LRRK2激酶抑制剂的情况下,在星形胶质细胞模型中评估了雷帕霉素哺乳动物靶标(mTOR)/Unc-51样激酶1(ULK1)和Beclin-1/磷脂酰肌醇3激酶(PI3K)途径。LRRK2激酶活性的化学抑制以非经典方式刺激巨自噬,独立于mTOR和ULK1,但依赖于含Beclin 1的III类PI3激酶的激活。