Changes in DNA binding pattern of transcription factor YY1 in neuronal degeneration

Molecular events under the neuronal degeneration are widely studied but still not defined. Here we compared the effects of both excitotoxic and apoptotic insults on the DNA binding profile of multifunctional transcription factor YY1 protein in cultured cerebellar granule neurons. We report that l-gl...

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Bibliographic Details
Published in:Neuroscience letters 2005-03, Vol.377 (2), p.121-124
Main Authors: Korhonen, Pauliina, Kyrylenko, Sergiy, Suuronen, Tiina, Salminen, Antero
Format: Article
Language:English
Subjects:
Aging
Animals
Apoptosis
Apoptosis - physiology
Biological and medical sciences
Calcium signalling
Cells, Cultured
Cerebellum - metabolism
DNA - genetics
DNA - metabolism
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Erythroid-Specific DNA-Binding Factors
Excitotoxicity
Fundamental and applied biological sciences. Psychology
Nerve Degeneration - genetics
Nerve Degeneration - metabolism
Neurodegeneration
Protein Binding - physiology
Rats
Transcription Factors - genetics
Transcription Factors - metabolism
Vertebrates: nervous system and sense organs
YY1 Transcription Factor
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Summary:Molecular events under the neuronal degeneration are widely studied but still not defined. Here we compared the effects of both excitotoxic and apoptotic insults on the DNA binding profile of multifunctional transcription factor YY1 protein in cultured cerebellar granule neurons. We report that l-glutamate-induced excitotoxic insult but not ionophore A23187 treatment caused the disappearance of the larger DNA binding complex of YY1 and a simultaneous appearance of the smaller YY1 complex in cerebellar granule neurons. MK-801 (NMDA receptor antagonist) as well as benzamide (PARP inhibitor), MDL 28170 (calpain inhibitor) and roscovitine (cyclin-dependent kinase inhibitor) inhibited the glutamate response to the YY1 complexes. Herbimycin, PD169316, wortmannin, JAK3 inhibitor, KN-93, H-7 and LY294002 were not effective. Apoptosis induced by okadaic acid but not that induced by etoposide or trichostatin A caused a similar excitotoxic reorganization in YY1 complexes. We suggest that despite the different cell death mechanisms, glutamate and okadaic acid activate signalling cascades that affect the formation of YY1 complexes and probably YY1-mediated gene regulation.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2004.11.085