Axon regeneration requires coordinate activation of p38 and JNK MAPK pathways

被引：160

作者：

Nix, Paola ^{[1
]}

Hisamoto, Naoki ^{[2
]}

Matsumoto, Kunihiro ^{[2
]}

Bastiani, Michael ^{[1
]}

机构：

[1] Univ Utah, Dept Biol, Salt Lake City, UT 84112 USA

[2] Nagoya Univ, Grad Sch Sci, Inst Adv Res, Dept Mol Biol, Nagoya, Aichi 4648602, Japan

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2011年 / 108卷 / 26期

基金：

美国国家科学基金会;

关键词：

Caenorhabditis elegans; MAPK signaling; laser axotomy; SPINAL-CORD-INJURY; CAENORHABDITIS-ELEGANS; C; ELEGANS; KINASE PATHWAY; DLK-1; KINASE; GROWTH; SIGNAL; ADULT; MICROFLUIDICS; NEUROSURGERY;

D O I：

10.1073/pnas.1104830108

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Signaling pathways essential for axon regeneration, but not for neuron development or function, are particularly well suited targets for therapeutic intervention. We find that the parallel PMK-3(p38) and KGB-1(JNK) MAPK pathways must be coordinately activated to promote axon regeneration. Axon regeneration fails if the activity of either pathway is absent. These two MAPKs are coregulated by the E3 ubiquitin ligase RPM-1(Phr1) via targeted degradation of the MAPKKKs DLK-1 and MLK-1 and by the MAPK phosphatase VHP-1(MKP7), which negatively regulates both PMK-3 (p38) and KGB-1(JNK).

引用

页码：10738 / 10743

页数：6

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