cAMP-response element-binding protein contributes to suppression of the A2A adenosine receptor promoter by mutant Huntingtin with expanded polyglutamine residues.

@article{Chiang2005cAMPresponseEP,
  title={cAMP-response element-binding protein contributes to suppression of the A2A adenosine receptor promoter by mutant Huntingtin with expanded polyglutamine residues.},
  author={Ming-Chang Chiang and Yi-Chao Lee and C L Huang and Yijuang Chern},
  journal={The Journal of biological chemistry},
  year={2005},
  volume={280 14},
  pages={14331-40}
}
Huntington's disease is a neurodegenerative disease resulting from a CAG (glutamine) trinucleotide expansion in exon 1 of the Huntingtin (Htt) gene. The role of the striatum-enriched A2A adenosine receptor (A2A-R) in Huntington's disease has attracted much attention lately. In the present study, we found that expression of mutant Htt with expanded poly(Q) significantly reduced the transcript levels of the endogenous A2A-R in PC12 cells and primary striatal neurons. Cotransfection of various… CONTINUE READING

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