Targeting the JNK Signaling Pathway for Stroke and Parkinson's Diseases Therapy

被引：92

作者：

Kuan, Chia-Yi ^{[1
]}

Burke, Robert E. ^{[2
]}

机构：

[1] Cincinnati Childrens Hosp Res Fdn, Div Dev Biol, TCHRF3464,3333 Burnet Ave, Cincinnati, OH 45229 USA

[2] Columbia Univ, Dept Neurol & Pathol, New York, NY 10032 USA

来源：

CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS | 2005年 / 4卷 / 01期

关键词：

D O I：

10.2174/1568007053005145

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：63 / 67

页数：5

共 46 条

[1] Identification of the critical features of a small peptide inhibitor of JNK activity [J].

Barr, RK ;

Kendrick, TS ;

Bogoyevitch, MA .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (13) :10987-10997

[2] Characterization of the c-Jun N-terminal kinase-BimEL signaling pathway in neuronal apoptosis [J].

Becker, EBE ;

Howell, J ;

Kodama, Y ;

Barker, PA ;

Bonni, A .

JOURNAL OF NEUROSCIENCE, 2004, 24 (40) :8762-8770

[3] Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation [J].

Behrens, A ;

Sibilia, M ;

Wagner, EF .

NATURE GENETICS, 1999, 21 (03) :326-329

[4] SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase [J].

Bennett, BL ;

Sasaki, DT ;

Murray, BW ;

O'Leary, EC ;

Sakata, ST ;

Xu, WM ;

Leisten, JC ;

Motiwala, A ;

Pierce, S ;

Satoh, Y ;

Bhagwat, SS ;

Manning, AM ;

Anderson, DW .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (24) :13681-13686

[5]

Bogoyevitch M.A, 2004, BIOCHIM BIOPHYS ACTA, V697, P89

[6] A peptide inhibitor of c-Jun N-terminal kinase protects against excitotoxicity and cerebral ischemia [J].

Borsello, T ;

Clarke, PGH ;

Hirt, L ;

Vercelli, A ;

Repici, M ;

Schorderet, DF ;

Bogousslavsky, J ;

Bonny, C .

NATURE MEDICINE, 2003, 9 (09) :1180-1186

[7] AS601245 (1,3-benzothiazol-2-yl(2-{[2-(3-pyridinyl)ethyl]amino}-4 pyrimidinyl) acetonitrile):: A c-Jun NH2-terminal protein kinase inhibitor with neuroprotective properties [J].

Carboni, S ;

Hiver, A ;

Szyndralewiez, C ;

Gaillard, P ;

Gotteland, JP ;

Vitte, PA .

JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2004, 310 (01) :25-32

[8] JNK-dependent release of mitochondrial protein, Smac, during apoptosis in multiple myeloma (MM) cells [J].

Chauhan, D ;

Li, GL ;

Hideshima, T ;

Podar, K ;

Mitsiades, C ;

Mitsiades, N ;

Munshi, N ;

Kharbanda, S ;

Anderson, KC .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (20) :17593-17596

[9] Signal transduction by the JNK group of MAP kinases [J].

Davis, RJ .

CELL, 2000, 103 (02) :239-252

[10] JNK1 - A PROTEIN-KINASE STIMULATED BY UV-LIGHT AND HA-RAS THAT BINDS AND PHOSPHORYLATES THE C-JUN ACTIVATION DOMAIN [J].

DERIJARD, B ;

HIBI, M ;

WU, IH ;

BARRETT, T ;

SU, B ;

DENG, TL ;

KARIN, M ;

DAVIS, RJ .

CELL, 1994, 76 (06) :1025-1037

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