The role of Epac proteins, novel cAMP mediators, in the regulation of immune, lung and neuronal function

作者: Maria Grandoch , Sara S. Roscioni , Martina Schmidt

DOI: 10.1111/J.1476-5381.2009.00458.X

关键词:

摘要: Chronic degenerative inflammatory diseases, such as chronic obstructive pulmonary disease and Alzheimer's dementia, afflict millions of people around the world, causing death debilitation. Despite global impact these there have been few innovative breakthroughs into their cause, treatment or cure. As with many debilitating disorders, diseases may be associated defective dysfunctional responses to second messengers, cyclic adenosinemonophosphate (cAMP). The identification cAMP-activated guanine nucleotide exchange factors for Ras-like GTPases, Epac1 (also known cAMP-GEF-I) Epac2 cAMP-GEF-II), profoundly altered prevailing assumptions concerning cAMP signalling, which until then had solely protein kinase A (PKA). Studies molecular mechanisms Epac-related signalling demonstrated that novel sensors regulate physiological processes either alone and/or in concert PKA. These include calcium handling, cardiac smooth muscle contraction, learning memory, cell proliferation differentiation, apoptosis, inflammation. diverse properties might explained by spatio-temporal compartmentalization, well A-kinase anchoring proteins, seem coordinate Epac networks. Future research should focus on Epac-regulated dynamics cAMP, and, hopefully, development compounds specifically interfere system order determine precise significance proteins disorders.

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