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Review ArticleReview Article

Adenosine Kinase: Exploitation for Therapeutic Gain

Detlev Boison
Stephen P.H. Alexander, ASSOCIATE EDITOR
Pharmacological Reviews July 2013, 65 (3) 906-943; DOI: https://doi.org/10.1124/pr.112.006361
Detlev Boison
Robert Stone Dow Neurobiology Laboratories, Legacy Research Institute, Portland, Oregon
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Stephen P.H. Alexander
Robert Stone Dow Neurobiology Laboratories, Legacy Research Institute, Portland, Oregon
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Abstract

Adenosine kinase (ADK; EC 2.7.1.20) is an evolutionarily conserved phosphotransferase that converts the purine ribonucleoside adenosine into 5′-adenosine-monophosphate. This enzymatic reaction plays a fundamental role in determining the tone of adenosine, which fulfills essential functions as a homeostatic and metabolic regulator in all living systems. Adenosine not only activates specific signaling pathways by activation of four types of adenosine receptors but it is also a primordial metabolite and regulator of biochemical enzyme reactions that couple to bioenergetic and epigenetic functions. By regulating adenosine, ADK can thus be identified as an upstream regulator of complex homeostatic and metabolic networks. Not surprisingly, ADK dysfunction is involved in several pathologies, including diabetes, epilepsy, and cancer. Consequently, ADK emerges as a rational therapeutic target, and adenosine-regulating drugs have been tested extensively. In recent attempts to improve specificity of treatment, localized therapies have been developed to augment adenosine signaling at sites of injury or pathology; those approaches include transplantation of stem cells with deletions of ADK or the use of gene therapy vectors to downregulate ADK expression. More recently, the first human mutations in ADK have been described, and novel findings suggest an unexpected role of ADK in a wider range of pathologies. ADK-regulating strategies thus represent innovative therapeutic opportunities to reconstruct network homeostasis in a multitude of conditions. This review will provide a comprehensive overview of the genetics, biochemistry, and pharmacology of ADK and will then focus on pathologies and therapeutic interventions. Challenges to translate ADK-based therapies into clinical use will be discussed critically.

Footnotes

  • This work was funded by the National Institutes of Health National Institute of Neurologic Disorders and Stroke [Grants NS061844, NS065957]; the National Institutes of Health National Institute of Mental Health [Grant MH083973]; the US Department of the Army (USAMRMC–PRMRP) [Contract W81XWH-12-1-0283]; the Parkinson’s Northwest Group; and the Legacy Hospital Foundations.

  • dx.doi.org/10.1124/pr.112.006361

  • Copyright © 2013 by The American Society for Pharmacology and Experimental Therapeutics
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Pharmacological Reviews: 65 (3)
Pharmacological Reviews
Vol. 65, Issue 3
1 Jul 2013
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Review ArticleReview Article

Adenosine Kinase

Detlev Boison
Pharmacological Reviews July 1, 2013, 65 (3) 906-943; DOI: https://doi.org/10.1124/pr.112.006361

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Review ArticleReview Article

Adenosine Kinase

Detlev Boison
Pharmacological Reviews July 1, 2013, 65 (3) 906-943; DOI: https://doi.org/10.1124/pr.112.006361
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    • Abstract
    • I. Introduction
    • II. Gene Structure and Transcription
    • III. Biochemistry
    • IV. Pharmacology
    • V. Physiology and Pathophysiology
    • VI. Therapeutic Applications of Adenosine Kinase-Based Interventions
    • VII. Implications for Human Pathogens
    • VIII. Conclusions and Outlook
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