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Molecular Pharmacology

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Research ArticleArticle

Rescue of p53 Blockage by the A2A Adenosine Receptor via a Novel Interacting Protein, Translin-Associated Protein X

Chung-Nan Sun, Hsiao-Chun Cheng, Jui-ling Chou, Shen-Yang Lee, Ya-Wen Lin, Hsing-Lin Lai, Hui-Mei Chen and Yijuang Chern
Molecular Pharmacology August 2006, 70 (2) 454-466; DOI: https://doi.org/10.1124/mol.105.021261
Chung-Nan Sun
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Hsiao-Chun Cheng
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Jui-ling Chou
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Shen-Yang Lee
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Ya-Wen Lin
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Hsing-Lin Lai
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Hui-Mei Chen
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Yijuang Chern
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Abstract

Blockage of the p53 tumor suppressor has been found to impair nerve growth factor (NGF)-induced neurite outgrowth in PC-12 cells. We report herein that such impairment could be rescued by stimulation of the A2A adenosine receptor (A2A-R), a G protein-coupled receptor implicated in neuronal plasticity. The A2A-R-mediated rescue occurred in the presence of protein kinase C (PKC) inhibitors or protein kinase A (PKA) inhibitors and in a PKA-deficient PC-12 variant. Thus, neither PKA nor PKC was involved. In contrast, expression of a truncated A2A-R mutant harboring the seventh transmembrane domain and its C terminus reduced the rescue effect of A2A-R. Using the cytoplasmic tail of the A2A-R as bait, a novel-A2A-R-interacting protein [translin-associated protein X (TRAX)] was identified in a yeast two-hybrid screen. The authenticity of this interaction was verified by pull-down experiments, coimmunoprecipitation, and colocalization of these two molecules in the brain. It is noteworthy that reduction of TRAX using an antisense construct suppressed the rescue effect of A2A-R, whereas overexpression of TRAX alone caused the same rescue effect as did A2A-R activation. Results of [3H]thymidine and bromodeoxyuridine incorporation suggested that A2A-R stimulation inhibited cell proliferation in a TRAX-dependent manner. Because the antimitotic activity is crucial for NGF function, the A2A-R might exert its rescue effect through a TRAX-mediated antiproliferative signal. This antimitotic activity of the A2A-R also enables a mitogenic factor (epidermal growth factor) to induce neurite outgrowth. We demonstrate that the A2A-R modulates the differentiation ability of trophic factors through a novel interacting protein, TRAX.

  • Received November 29, 2005.
  • Accepted April 14, 2006.
  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 70 (2)
Molecular Pharmacology
Vol. 70, Issue 2
1 Aug 2006
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Research ArticleArticle

Rescue of p53 Blockage by the A2A Adenosine Receptor via a Novel Interacting Protein, Translin-Associated Protein X

Chung-Nan Sun, Hsiao-Chun Cheng, Jui-ling Chou, Shen-Yang Lee, Ya-Wen Lin, Hsing-Lin Lai, Hui-Mei Chen and Yijuang Chern
Molecular Pharmacology August 1, 2006, 70 (2) 454-466; DOI: https://doi.org/10.1124/mol.105.021261

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Research ArticleArticle

Rescue of p53 Blockage by the A2A Adenosine Receptor via a Novel Interacting Protein, Translin-Associated Protein X

Chung-Nan Sun, Hsiao-Chun Cheng, Jui-ling Chou, Shen-Yang Lee, Ya-Wen Lin, Hsing-Lin Lai, Hui-Mei Chen and Yijuang Chern
Molecular Pharmacology August 1, 2006, 70 (2) 454-466; DOI: https://doi.org/10.1124/mol.105.021261
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