Abstract
The signaling pathways which contribute to neuronal death during development, aging and disease have been extensively studied. While initial efforts focused on developmental death, increasing evidence suggests that mitogenactivated protein kinase pathways play a role in human pathology. In particular, the c-Jun N-terminal kinases (JNKs), mitogen- activated protein kinases activated by extracellular stimuli including stress, are a major focus. Knock-out mouse studies have demonstrated that removing particular JNK genes can reduce the severity in various disease scenarios, including those which are used to model Parkinsons disease and cerebral ischemia. In addition, activation of JNKs can be seen in human disease tissue. In this review we bring together the evidence for JNK being an important regulator of neuronal loss and outline the advancement of small molecule inhibitors for future therapeutic intervention.
Keywords: Mitogen-activated protein kinase, c-Jun N-terminal kinase, phosphorylation, neurodegeneration, Alzheimer's disease, Parkinson's disease, neuroprotection
CNS & Neurological Disorders - Drug Targets
Title: MAP Kinase Pathways in Neuronal Cell Death
Volume: 7 Issue: 1
Author(s): Karen L. Philpott and Laura Facci
Affiliation:
Keywords: Mitogen-activated protein kinase, c-Jun N-terminal kinase, phosphorylation, neurodegeneration, Alzheimer's disease, Parkinson's disease, neuroprotection
Abstract: The signaling pathways which contribute to neuronal death during development, aging and disease have been extensively studied. While initial efforts focused on developmental death, increasing evidence suggests that mitogenactivated protein kinase pathways play a role in human pathology. In particular, the c-Jun N-terminal kinases (JNKs), mitogen- activated protein kinases activated by extracellular stimuli including stress, are a major focus. Knock-out mouse studies have demonstrated that removing particular JNK genes can reduce the severity in various disease scenarios, including those which are used to model Parkinsons disease and cerebral ischemia. In addition, activation of JNKs can be seen in human disease tissue. In this review we bring together the evidence for JNK being an important regulator of neuronal loss and outline the advancement of small molecule inhibitors for future therapeutic intervention.
Export Options
About this article
Cite this article as:
Philpott L. Karen and Facci Laura, MAP Kinase Pathways in Neuronal Cell Death, CNS & Neurological Disorders - Drug Targets 2008; 7 (1) . https://dx.doi.org/10.2174/187152708783885129
DOI https://dx.doi.org/10.2174/187152708783885129 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Dry Age-Related Macular Degeneration: Recent Progress of Therapeutic approaches
Current Molecular Pharmacology Microglial Integrity is Maintained by Erythropoietin Through Integration of Akt and Its Substrates of lycogen Synthase Kinase-3β, β-Catenin, and Nuclear Factor-κB
Current Neurovascular Research Anticancer Therapeutic Strategies Based on CDK Inhibitors
Current Pharmaceutical Design The Multifactorial Nature of Alzheimer's Disease for Developing Potential Therapeutics
Current Topics in Medicinal Chemistry Breaking the Barrier of Cancer Through Liposome Loaded with Phytochemicals
Current Drug Delivery Nanoparticles Based on Plasma Proteins for Drug Delivery Applications
Current Pharmaceutical Design Neuropeptide FF Inhibits LPS-Mediated Osteoclast Differentiation of RAW264.7 Cells
Protein & Peptide Letters Unique Medicinal Properties of Withania somnifera: Phytochemical Constituents and Protein Component
Current Pharmaceutical Design Platelet-Activating Factor (PAF) Antagonists Attenuate Inflammatory- Based Pain: Potential Cellular and Anatomical Sites of PAF Action
Central Nervous System Agents in Medicinal Chemistry Evolving Therapeutic Targets in Ischemic Stroke: A Concise Review
Current Drug Targets Recent Advances in Clarifying Prion Protein Functions Using Knockout Mice and Derived Cell Lines
Mini-Reviews in Medicinal Chemistry Channel-Like Functions of the 18-kDa Translocator Protein (TSPO): Regulation of Apoptosis and Steroidogenesis as Part of the Host-Defense Response
Current Pharmaceutical Design Epigenetic Modification in Neuropathic Pain
Current Pharmaceutical Design Fibroblast Growth Factor 2: From Laboratory Evidence to Clinical Application
Current Vascular Pharmacology Repurposing of Anti-Diabetic Agents for the Treatment of Cognitive Impairment and Mood Disorders
Current Molecular Medicine Opioid Withdrawal Syndrome: Emerging Concepts and Novel Therapeutic Targets
CNS & Neurological Disorders - Drug Targets MicroRNA Regulatory Network in Human Colorectal Cancer
Mini-Reviews in Medicinal Chemistry In vivo Real-Time Near-Infrared Fluorescent Mapping of Sentinel Lymph Nodes Using Methylene Blue Encapsulated in a Microemulsion Nanosystem
Current Nanoscience Withaferin A Regulates LRRK2 Levels by Interfering with the Hsp90- Cdc37 Chaperone Complex
Current Aging Science Redox-active and Redox-silent Compounds: Synergistic Therapeutics in Cancer
Current Medicinal Chemistry