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cAMP-PKA phosphorylation of tau confers risk for degeneration in aging association cortex.cAMP-PKA 对 tau 的磷酸化使衰老相关皮质中的退行性病变风险增加。
Proc Natl Acad Sci U S A. 2014 Apr 1;111(13):5036-41. doi: 10.1073/pnas.1322360111. Epub 2014 Mar 18.
2
Elevated MARK2-dependent phosphorylation of Tau in Alzheimer's disease.阿尔茨海默病中 Tau 依赖 MARK2 的磷酸化升高。
J Alzheimers Dis. 2013;33(3):699-713. doi: 10.3233/JAD-2012-121357.
3
Alzheimer's β-secretase (BACE1) regulates the cAMP/PKA/CREB pathway independently of β-amyloid.阿尔茨海默病 β-分泌酶（BACE1）独立于 β-淀粉样蛋白调节 cAMP/PKA/CREB 通路。
J Neurosci. 2012 Aug 15;32(33):11390-5. doi: 10.1523/JNEUROSCI.0757-12.2012.
4
A novel function of the cell polarity-regulating kinase PAR-1/MARK in dendritic spines.细胞极性调节激酶PAR-1/MARK在树突棘中的一种新功能。
Bioarchitecture. 2011 Nov 1;1(6):261-266. doi: 10.4161/bioa.1.6.19199.
5
PAR-1/MARK: a kinase essential for maintaining the dynamic state of microtubules.PAR-1/MARK：一种维持微管动态状态所必需的激酶。
Cell Struct Funct. 2012;37(1):21-5. doi: 10.1247/csf.11038. Epub 2011 Dec 3.
6
Interplay between microtubule dynamics and intracellular organization.微管动力学与细胞内组织的相互作用。
Int J Biochem Cell Biol. 2012 Feb;44(2):266-74. doi: 10.1016/j.biocel.2011.11.009. Epub 2011 Nov 17.
7
Neuronal polarization: the cytoskeleton leads the way.神经元极化：细胞骨架引领方向。
Dev Neurobiol. 2011 Jun;71(6):430-44. doi: 10.1002/dneu.20849.
8
DAPK activates MARK1/2 to regulate microtubule assembly, neuronal differentiation, and tau toxicity.DAPK 通过激活 MARK1/2 来调节微管组装、神经元分化和 tau 毒性。
Cell Death Differ. 2011 Sep;18(9):1507-20. doi: 10.1038/cdd.2011.2. Epub 2011 Feb 11.
9
Rewirable gene regulatory networks in the preimplantation embryonic development of three mammalian species.三种哺乳动物种系植入前胚胎发育中的可重设基因调控网络。
Genome Res. 2010 Jun;20(6):804-15. doi: 10.1101/gr.100594.109. Epub 2010 Mar 10.
10
Par1b/MARK2 phosphorylates kinesin-like motor protein GAKIN/KIF13B to regulate axon formation.Par1b/MARK2 通过磷酸化驱动蛋白样马达蛋白 GAKIN/KIF13B 来调节轴突形成。
Mol Cell Biol. 2010 May;30(9):2206-19. doi: 10.1128/MCB.01181-09. Epub 2010 Mar 1.

蛋白激酶A通过磷酸化丝氨酸409来挽救微管亲和力调节激酶2诱导的微管不稳定性和神经突破坏。

Protein kinase A rescues microtubule affinity-regulating kinase 2-induced microtubule instability and neurite disruption by phosphorylating serine 409.

作者信息

Deng Si-Si, Wu Le-Yu, Wang Ya-Chao, Cao Peng-Rong, Xu Lei, Li Qian-Ru, Liu Meng, Zhang Lun, Jiang Yue-Jing, Yang Xiao-Yu, Sun Sheng-Nan, Tan Min-jia, Qian Min, Zang Yi, Feng Linyin, Li Jia

机构信息

From the National Center for Drug Screening, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 189 Guo Shoujing Road, Shanghai 201203, China.

Department of Neuropharmacology, CAS Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zu Chong Zhi Road, Shanghai 201203, China.

出版信息

J Biol Chem. 2015 Jan 30;290(5):3149-60. doi: 10.1074/jbc.M114.629873. Epub 2014 Dec 15.

DOI:10.1074/jbc.M114.629873
PMID:25512381
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4317040/
Abstract

Microtubule affinity-regulating kinase 2 (MARK2)/PAR-1b and protein kinase A (PKA) are both involved in the regulation of microtubule stability and neurite outgrowth, but whether a direct cross-talk exists between them remains unclear. Here, we found the disruption of microtubule and neurite outgrowth induced by MARK2 overexpression was blocked by active PKA. The interaction between PKA and MARK2 was confirmed by coimmunoprecipitation and immunocytochemistry both in vitro and in vivo. PKA was found to inhibit MARK2 kinase activity by phosphorylating a novel site, serine 409. PKA could not reverse the microtubule disruption effect induced by a serine 409 to alanine (Ala) mutant of MARK2 (MARK2 S409A). In contrast, mutation of MARK2 serine 409 to glutamic acid (Glu) (MARK2 S409E) did not affect microtubule stability and neurite outgrowth. We propose that PKA functions as an upstream inhibitor of MARK2 in regulating microtubule stability and neurite outgrowth by directly interacting and phosphorylating MARK2.

摘要

微管亲和力调节激酶2（MARK2）/PAR-1b和蛋白激酶A（PKA）均参与微管稳定性和神经突生长的调节，但它们之间是否存在直接的相互作用尚不清楚。在此，我们发现由MARK2过表达诱导的微管和神经突生长的破坏被活性PKA所阻断。通过体外和体内的共免疫沉淀和免疫细胞化学证实了PKA与MARK2之间的相互作用。发现PKA通过磷酸化一个新位点丝氨酸409来抑制MARK2激酶活性。PKA不能逆转由MARK2的丝氨酸409突变为丙氨酸（Ala）的突变体（MARK2 S409A）诱导的微管破坏效应。相反，MARK2的丝氨酸409突变为谷氨酸（Glu）（MARK2 S409E）并不影响微管稳定性和神经突生长。我们提出PKA在通过直接与MARK2相互作用并使其磷酸化来调节微管稳定性和神经突生长中作为MARK2的上游抑制剂发挥作用。