![]() ![]() The generation of cAMP is initiated when an extracellular first messenger (neurotransmitter, hormone, chemokine, lipid mediator, or drug) binds to a seven transmembrane–spanning G protein–coupled receptor (GPCR) that is coupled to a stimulatory G protein α subunit (Gαs) ( Figure 1). Although many contemporary reviews on innate immunity focus on pathogen recognition receptors and signaling pathways ( 3), the importance of cAMP as a controller derives from its ability to exert broad modulatory effects that are independent of the pathogen, the recognition receptor, or the signaling pathway in question. This review will address cAMP regulation of innate immunity, with an emphasis on the lung. Biological processes mediated by this second messenger include memory, metabolism, gene regulation, and immune function ( 2). cAMP is now recognized as a universal regulator of cellular function in organisms including amoebas, plants, and humans ( 1). Sutherland was awarded the 1971 Nobel Prize for this work, which would prove to be the first of five Nobel Prizes recognizing research on this molecule. Sutherland during his studies of the mechanisms of hormone action. The cyclic nucleotide cyclic adenosine monophosphate (cAMP)-the original member of the family of second messengers-was discovered by Dr. This review will provide clinicians with an overview of the cyclic AMP axis, its role as a down-regulator of host antimicrobial defense functions, and the clinical and translational relevance of such actions. ![]()
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