JNK pathway as therapeutic target to prevent degeneration in the central nervous system

Mariaelena Repici, Tiziana Borsello

Research output: Contribution to journalReview article

Abstract

JNKs (c-Jun N- terminal kinases) are important transducing enzymes involved in many faces of cellular regulation such as gene expression, cell proliferation and programmed cell death. The activation of JNK pathway is critical for naturally occurring neuronal death during development as well as for pathological death of adult brain following different insults. In particular, JNKs play an important role in excitotoxicity and all related phenomena. Initial research concentrated on defining the components and organization of JNK signalling cascades, but more recent studies have begun to see JNK as the appropriate target for prevent cell loss. We used a specific JNK inhibitor, the cell permeable peptide D-JNKI1, to block JNK action in neuronal death following excitotoxicity in vitro and cerebral ischemia in vivo. Here we review our recent findings and we discuss the possibility of using D-JNKI1 as a therapeutic agent to prevent cell loss in the central nervous system.

Original languageEnglish
Pages (from-to)145-55
Number of pages11
JournalAdvances in Experimental Medicine and Biology
Volume588
Publication statusPublished - 2006

Fingerprint

JNK Mitogen-Activated Protein Kinases
Neurology
Central Nervous System
Therapeutics
Critical Pathways
Brain Death
Cell proliferation
Cell death
Brain Ischemia
Gene expression
Brain
Cell Death
Chemical activation
Cell Proliferation
Gene Expression
Peptides
Enzymes
Research

Keywords

  • Animals
  • Central Nervous System/physiology
  • Disease Models, Animal
  • Enzyme Inhibitors/pharmacology
  • Hippocampus/metabolism
  • Humans
  • Ischemia/pathology
  • MAP Kinase Kinase 4/metabolism
  • Mice
  • Nerve Degeneration/pathology
  • Neurodegenerative Diseases/pathology
  • Neurons/metabolism
  • Peptides/chemistry
  • Rats

Cite this

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title = "JNK pathway as therapeutic target to prevent degeneration in the central nervous system",
abstract = "JNKs (c-Jun N- terminal kinases) are important transducing enzymes involved in many faces of cellular regulation such as gene expression, cell proliferation and programmed cell death. The activation of JNK pathway is critical for naturally occurring neuronal death during development as well as for pathological death of adult brain following different insults. In particular, JNKs play an important role in excitotoxicity and all related phenomena. Initial research concentrated on defining the components and organization of JNK signalling cascades, but more recent studies have begun to see JNK as the appropriate target for prevent cell loss. We used a specific JNK inhibitor, the cell permeable peptide D-JNKI1, to block JNK action in neuronal death following excitotoxicity in vitro and cerebral ischemia in vivo. Here we review our recent findings and we discuss the possibility of using D-JNKI1 as a therapeutic agent to prevent cell loss in the central nervous system.",
keywords = "Animals, Central Nervous System/physiology, Disease Models, Animal, Enzyme Inhibitors/pharmacology, Hippocampus/metabolism, Humans, Ischemia/pathology, MAP Kinase Kinase 4/metabolism, Mice, Nerve Degeneration/pathology, Neurodegenerative Diseases/pathology, Neurons/metabolism, Peptides/chemistry, Rats",
author = "Mariaelena Repici and Tiziana Borsello",
year = "2006",
language = "English",
volume = "588",
pages = "145--55",
journal = "Advances in Experimental Medicine and Biology",
issn = "0065-2598",
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JNK pathway as therapeutic target to prevent degeneration in the central nervous system. / Repici, Mariaelena; Borsello, Tiziana.

In: Advances in Experimental Medicine and Biology, Vol. 588, 2006, p. 145-55.

Research output: Contribution to journalReview article

TY - JOUR

T1 - JNK pathway as therapeutic target to prevent degeneration in the central nervous system

AU - Repici, Mariaelena

AU - Borsello, Tiziana

PY - 2006

Y1 - 2006

N2 - JNKs (c-Jun N- terminal kinases) are important transducing enzymes involved in many faces of cellular regulation such as gene expression, cell proliferation and programmed cell death. The activation of JNK pathway is critical for naturally occurring neuronal death during development as well as for pathological death of adult brain following different insults. In particular, JNKs play an important role in excitotoxicity and all related phenomena. Initial research concentrated on defining the components and organization of JNK signalling cascades, but more recent studies have begun to see JNK as the appropriate target for prevent cell loss. We used a specific JNK inhibitor, the cell permeable peptide D-JNKI1, to block JNK action in neuronal death following excitotoxicity in vitro and cerebral ischemia in vivo. Here we review our recent findings and we discuss the possibility of using D-JNKI1 as a therapeutic agent to prevent cell loss in the central nervous system.

AB - JNKs (c-Jun N- terminal kinases) are important transducing enzymes involved in many faces of cellular regulation such as gene expression, cell proliferation and programmed cell death. The activation of JNK pathway is critical for naturally occurring neuronal death during development as well as for pathological death of adult brain following different insults. In particular, JNKs play an important role in excitotoxicity and all related phenomena. Initial research concentrated on defining the components and organization of JNK signalling cascades, but more recent studies have begun to see JNK as the appropriate target for prevent cell loss. We used a specific JNK inhibitor, the cell permeable peptide D-JNKI1, to block JNK action in neuronal death following excitotoxicity in vitro and cerebral ischemia in vivo. Here we review our recent findings and we discuss the possibility of using D-JNKI1 as a therapeutic agent to prevent cell loss in the central nervous system.

KW - Animals

KW - Central Nervous System/physiology

KW - Disease Models, Animal

KW - Enzyme Inhibitors/pharmacology

KW - Hippocampus/metabolism

KW - Humans

KW - Ischemia/pathology

KW - MAP Kinase Kinase 4/metabolism

KW - Mice

KW - Nerve Degeneration/pathology

KW - Neurodegenerative Diseases/pathology

KW - Neurons/metabolism

KW - Peptides/chemistry

KW - Rats

M3 - Review article

C2 - 17089886

VL - 588

SP - 145

EP - 155

JO - Advances in Experimental Medicine and Biology

JF - Advances in Experimental Medicine and Biology

SN - 0065-2598

ER -