Redox state-dependent gasocrine signaling

Abstract

I recently proposed the term 'gasocrine signaling' to describe a cell signaling event based on the binding of gaseous signaling molecules or gasotransmitters to gasoreceptor proteins. To investigate gasocrine signaling, it is essential to identify all the gasoreceptors for the gases generated in a cell or that reach a cell. Proteins can undergo gas-dependent changes in redox states, regulating protein disulfide bond formation or cleavage. Protein disulfide bonds play a pivotal role in protein folding, stability, localization, cellular signaling, function and the evolution of life. Drawing an analogy with the wicket rule of Cricket, where a batsman is dismissed upon bail dislodgement, I propose that the redox states of proteins with signaling or transcriptional activities, dependent on gaseous signaling molecules or gasotransmitters, be termed simply as 'gasoreceptor activation states’. I propose E. coli SoxR is a gasoreceptor with transcriptional activities, while mammalian VEGFR2 kinase and CD36 fatty acid transporter represent other classes of gasoreceptors. Embracing the complexity and diversity of gasoreceptors will facilitate a systematic exploration of the almost infinite number of gasoreceptors and their role in gasocrine signaling. Finally, I propose a modification of the definition of 'gasocrine signaling' to ‘a cell signaling event based on the interaction of gaseous signaling molecules or gasotransmitters to gasoreceptor proteins’.