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Biological functions of ecto-enzymes in regulating extracellular adenosine levels in neoplastic and inflammatory disease states.
MedLine Citation:
PMID:  23292173     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
When present in the extracellular environment, the nucleoside adenosine protects cells and tissues from excessive inflammation and immune-mediated damage while promoting healing processes. This role has been highlighted experimentally using distinct disease models, including those of colitis, diabetes, asthma, sepsis, and ischemic injury. Adenosine also suppresses immune responses, as in the tumor microenvironment, assisting immune evasion while promoting angiogenesis. The mechanisms involved in adenosine signaling are addressed elsewhere in this issue. Here, the authors specifically address the generation of adenosine from extracellular nucleotides. This process is catalyzed by a series of plasma membrane ectonucleotidases, with the focus in this article on members of the CD39, CD73, and CD38 families and on their role in inflammatory and neoplastic hematological diseases. Pharmacological modulation of adenosine generation by drugs that either have or modulate ectonucleotidase function might be exploited to treat these diverse conditions.
Authors:
Maria Serena Longhi; Simon C Robson; Steven H Bernstein; Sara Serra; Silvia Deaglio
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-1-6
Journal Detail:
Title:  Journal of molecular medicine (Berlin, Germany)     Volume:  -     ISSN:  1432-1440     ISO Abbreviation:  J. Mol. Med.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-1-7     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9504370     Medline TA:  J Mol Med (Berl)     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Institute of Liver Studies, King's College London School of Medicine at King's College Hospital, Denmark Hill, SE5 9RS, London, UK, maria.longhi@kcl.ac.uk.
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