Literature DB >> 15723614

Targeting the JNK signaling pathway for stroke and Parkinson's diseases therapy.

Chia-Yi Kuan1, Robert E Burke.   

Abstract

The c-Jun NH2-terminal Kinase (JNK) signaling pathway is frequently induced by cellular stress and correlated with neuronal death. This unique property makes JNK signaling a promising target for developing pharmacological intervention. Among several neurological disorders, JNK signaling is particularly implicated in ischemic stroke and Parkinson's disease. The inhibitors of the JNK signaling pathway include upstream kinase inhibitors (for example, CEP-1347), small chemical inhibitors of JNK (SP600125 and AS601245), and peptide inhibitors of the interaction between JNK and its substrates (D-JNKI and I-JIP). The mechanisms by which JNK signaling induces apoptosis and evidence of cytoprotective effects of these JNK inhibitors are summarized in the present review.

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Year:  2005        PMID: 15723614     DOI: 10.2174/1568007053005145

Source DB:  PubMed          Journal:  Curr Drug Targets CNS Neurol Disord        ISSN: 1568-007X


  30 in total

Review 1.  The c-jun kinase/stress-activated pathway: regulation, function and role in human disease.

Authors:  Gary L Johnson; Kazuhiro Nakamura
Journal:  Biochim Biophys Acta       Date:  2007-01-04

2.  Glutathione S-transferase pi mediates MPTP-induced c-Jun N-terminal kinase activation in the nigrostriatal pathway.

Authors:  Margarida Castro-Caldas; Andreia Neves Carvalho; Elsa Rodrigues; Colin Henderson; C Roland Wolf; Maria João Gama
Journal:  Mol Neurobiol       Date:  2012-04-27       Impact factor: 5.590

Review 3.  Mitochondrial kinases in Parkinson's disease: converging insights from neurotoxin and genetic models.

Authors:  Ruben K Dagda; Jianhui Zhu; Charleen T Chu
Journal:  Mitochondrion       Date:  2009-06-27       Impact factor: 4.160

Review 4.  Brain angiogenesis in developmental and pathological processes: neurovascular injury and angiogenic recovery after stroke.

Authors:  Ken Arai; Guang Jin; Deepti Navaratna; Eng H Lo
Journal:  FEBS J       Date:  2009-07-31       Impact factor: 5.542

Review 5.  JNK signalling in cancer: in need of new, smarter therapeutic targets.

Authors:  Concetta Bubici; Salvatore Papa
Journal:  Br J Pharmacol       Date:  2014-01       Impact factor: 8.739

6.  Unraveling the neuroprotective mechanisms of PrP (C) in excitotoxicity.

Authors:  Franc Llorens; José Antonio Del Río
Journal:  Prion       Date:  2012-07-01       Impact factor: 3.931

7.  Sh3rf2/POSHER protein promotes cell survival by ring-mediated proteasomal degradation of the c-Jun N-terminal kinase scaffold POSH (Plenty of SH3s) protein.

Authors:  Michael Wilhelm; Nickolay V Kukekov; Travis L Schmit; Katherine V Biagas; Andrew A Sproul; Stephen Gire; Margaret E Maes; Zhiheng Xu; Lloyd A Greene
Journal:  J Biol Chem       Date:  2011-11-28       Impact factor: 5.157

Review 8.  Cell cycle inhibition without disruption of neurogenesis is a strategy for treatment of central nervous system diseases.

Authors:  Da-Zhi Liu; Bradley P Ander; Frank R Sharp
Journal:  Neurobiol Dis       Date:  2009-11-24       Impact factor: 5.996

9.  Tumor necrosis factor-alpha-induced sickness behavior is impaired by central administration of an inhibitor of c-jun N-terminal kinase.

Authors:  K Palin; R H McCusker; K Strle; F Moos; R Dantzer; K W Kelley
Journal:  Psychopharmacology (Berl)       Date:  2008-02-12       Impact factor: 4.530

10.  ULK1 and JNK are involved in mitophagy incurred by LRRK2 G2019S expression.

Authors:  Yuangang Zhu; Chunyan Wang; Mei Yu; Jie Cui; Liang Liu; Zhiheng Xu
Journal:  Protein Cell       Date:  2013-09-10       Impact factor: 14.870

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