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Transactivation of receptor tyrosine kinases by purinergic P2Y and adenosine receptors

Transactivation of receptor tyrosine kinases by purinergic P2Y and adenosine receptors Transactivation of receptor tyrosine kinases (RTK) is a crosstalk mechanism exhibited by G-protein–coupled receptors (GPCR) to activate signaling pathways classically associated with growth factors. The discovery of RTK transactivation was a breakthrough in signal transduction that contributed to developing current concepts in intracellular signaling. RTK transactivation links GPCR signaling to important cellular processes, such as cell proliferation and differentiation, and explains the functional diversity of these receptors. Purinergic (P2Y and adenosine) receptors belong to class A of GPCR; in the present work, we systematically review the experimental evidence showing that purinergic receptors have the ability to transactivate RTK in multiple tissues and physiopathological conditions resulting in the modulation of cellular physiology. Of particular relevance, the crosstalk between purinergic receptors and epidermal growth factor receptor is a redundant pathway that participates in multiple pathophysiological processes. Specific and detailed knowledge of purinergic receptor-regulated pathways advances our understanding of the complexity of GPCR signal transduction and opens the way for pharmacologic intervention in the pathological context. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Purinergic Signalling Springer Journals

Transactivation of receptor tyrosine kinases by purinergic P2Y and adenosine receptors

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References (72)

Publisher
Springer Journals
Copyright
Copyright © The Author(s), under exclusive licence to Springer Nature B.V. 2022. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
ISSN
1573-9538
eISSN
1573-9546
DOI
10.1007/s11302-022-09913-y
Publisher site
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Abstract

Transactivation of receptor tyrosine kinases (RTK) is a crosstalk mechanism exhibited by G-protein–coupled receptors (GPCR) to activate signaling pathways classically associated with growth factors. The discovery of RTK transactivation was a breakthrough in signal transduction that contributed to developing current concepts in intracellular signaling. RTK transactivation links GPCR signaling to important cellular processes, such as cell proliferation and differentiation, and explains the functional diversity of these receptors. Purinergic (P2Y and adenosine) receptors belong to class A of GPCR; in the present work, we systematically review the experimental evidence showing that purinergic receptors have the ability to transactivate RTK in multiple tissues and physiopathological conditions resulting in the modulation of cellular physiology. Of particular relevance, the crosstalk between purinergic receptors and epidermal growth factor receptor is a redundant pathway that participates in multiple pathophysiological processes. Specific and detailed knowledge of purinergic receptor-regulated pathways advances our understanding of the complexity of GPCR signal transduction and opens the way for pharmacologic intervention in the pathological context.

Journal

Purinergic Signalling – Springer Journals

Published: Dec 19, 2022

Keywords: Purinergic receptors; GPCR; Transactivation; EGFR; P2Y receptor; Adenosine receptors; RTK

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