Bcl-2 enhances neurite extension via activation of c-Jun N-terminal kinase

Dae Seok Eom, Won Seok Choi, Young Jun Oh

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Recent studies suggest that Bcl-2 may play an active role in neuronal differentiation. Here, we showed a marked neurite extension in MN9D dopaminergic neuronal cells overexpressing Bcl-2 (MN9D/Bcl-2) or Bcl-X L (MN9D/Bcl-XL). We found a specific increase in phosphorylation of c-Jun N-terminal kinase (JNK) accompanied by neurite extension in MN9D/Bcl-2 but not in MN9D/Bcl-XL cells. Consequently, neurite extension in MN9D/Bcl-2 but not in MN9D/Bcl-XL cells was suppressed by treatment with SP600125, a specific inhibitor of JNK. Inhibition of other mitogen-activated protein kinases - including p38 and extracellular signal-regulated kinase - did not affect Bcl-2-mediated neurite extension in MN9D cells. While the expression levels of such protein markers of maturation as SNAP-25, phosphorylated NF-H, and neuron-specific enolase were increased in MN9D/Bcl-2 cells, only upregulation of SNAP-25 was inhibited after treatment with SP600125. Thus, the JNK signal activated by Bcl-2 seems to play an important role during morphological and certain biochemical differentiation in cultured dopaminergic neurons.

Original languageEnglish
Pages (from-to)377-381
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume314
Issue number2
DOIs
Publication statusPublished - 2004 Feb 6

Fingerprint

JNK Mitogen-Activated Protein Kinases
Neurites
Chemical activation
Phosphorylation
Phosphopyruvate Hydratase
Extracellular Signal-Regulated MAP Kinases
Mitogen-Activated Protein Kinases
Neurons
Dopaminergic Neurons
Proteins
p38 Mitogen-Activated Protein Kinases
Up-Regulation
anthra(1,9-cd)pyrazol-6(2H)-one

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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title = "Bcl-2 enhances neurite extension via activation of c-Jun N-terminal kinase",
abstract = "Recent studies suggest that Bcl-2 may play an active role in neuronal differentiation. Here, we showed a marked neurite extension in MN9D dopaminergic neuronal cells overexpressing Bcl-2 (MN9D/Bcl-2) or Bcl-X L (MN9D/Bcl-XL). We found a specific increase in phosphorylation of c-Jun N-terminal kinase (JNK) accompanied by neurite extension in MN9D/Bcl-2 but not in MN9D/Bcl-XL cells. Consequently, neurite extension in MN9D/Bcl-2 but not in MN9D/Bcl-XL cells was suppressed by treatment with SP600125, a specific inhibitor of JNK. Inhibition of other mitogen-activated protein kinases - including p38 and extracellular signal-regulated kinase - did not affect Bcl-2-mediated neurite extension in MN9D cells. While the expression levels of such protein markers of maturation as SNAP-25, phosphorylated NF-H, and neuron-specific enolase were increased in MN9D/Bcl-2 cells, only upregulation of SNAP-25 was inhibited after treatment with SP600125. Thus, the JNK signal activated by Bcl-2 seems to play an important role during morphological and certain biochemical differentiation in cultured dopaminergic neurons.",
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Bcl-2 enhances neurite extension via activation of c-Jun N-terminal kinase. / Eom, Dae Seok; Choi, Won Seok; Oh, Young Jun.

In: Biochemical and Biophysical Research Communications, Vol. 314, No. 2, 06.02.2004, p. 377-381.

Research output: Contribution to journalArticle

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