Targeting Strategies to Modulate the NF-κB and JNK Signal Transduction Network

ISSN: 1875-614X (Online)
ISSN: 1871-5230 (Print)


Volume 15, 3 Issues, 2016


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Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Inflammatory and Anti-Allergy Agents

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Editor-in-Chief:
Claudiu T. Supuran
Neurofarba Department
University of Florence
Florence
Italy


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Targeting Strategies to Modulate the NF-κB and JNK Signal Transduction Network



Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry, 6(1): 71-84.

Author(s): Michael Kracht.

Affiliation: Institute of Pharmacology,Medical School Hannover, Carl Neuberg Strasse 1, D-30625 Hannover,Germany.

Abstract

The signal transduction pathways leading to activation of Jun-NH2-terminal kinase (JNK) and nuclear factor- κB (NF-κB) are activated by a plethora of extracellular signals. Small molecules have been developed that inhibit the JNK or IκB protein kinases. Additionally, several cell-penetrating peptides have been characterized that disrupt proteinprotein interaction domains within the NF-κB and JNK signalling pathways. Usually NF-κB and JNK are (re)viewed as separate signalling systems. However, emerging evidence suggests that both pathways are interconnected at various levels. In this review, the spatiotemporal control of JNK or NF-κ B activation is discussed in conjunction with cross talk mechanisms and various regulatory feedback loops. A detailed understanding of these mechanisms is important to optimize available strategies to interfere with NF-κB or JNK signalling.

Keywords:

chromatin-immunoprecipitation (ChIP), MAP kinase kinase kinases (MAKKK), ATP-competitve inhibitors, c-JUN Docking Sites, tumor necrosis factor.



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Article Details

Volume: 6
Issue Number: 1
First Page: 71
Last Page: 84
Page Count: 14
DOI: 10.2174/187152307779939705
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