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There are three basic types of secondary messenger molecules: [citation needed] Hydrophobic molecules: water-insoluble molecules such as diacylglycerol, and phosphatidylinositols, which are membrane-associated and diffuse from the plasma membrane into the intermembrane space where they can reach and regulate membrane-associated effector proteins.
Cyclic di-AMP (also called c-di-AMP and c-di-adenosine monophosphate) is a second messenger used in signal transduction in bacteria and archaea. [1] [2] [3] It is present in many Gram-positive bacteria, some Gram-negative species, and archaea of the phylum Euryarchaeota.
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Following activation of adenylyl cyclase, the resulting cAMP acts as a second messenger by interacting with and regulating other proteins such as protein kinase A and cyclic nucleotide-gated ion channels. [11] Photoactivated adenylyl cyclase (PAC) was discovered in Euglena gracilis and can be expressed in other organisms through genetic ...
Diguanylate cyclase participate in the formation of the ubiquitous second messenger, cyclic-di-GMP, involved in bacterial biofilm formation and persistence. The GGDEF domain was first identified in the regulatory protein, PleD of the bacterium Caulobacter crescentus. [6]
A bacteriophage that infects C. difficile is predicted to carry a cyclic di-GMP-I riboswitch, which it might use to detect and exploit the physiological state of bacteria that it infects. The discovery of this riboswitch class answers the question of how genes are regulated in response to cyclic di-GMP levels in many different bacteria.
It acts as a coenzyme in redox reactions, as a donor of ADP-ribose moieties in ADP-ribosylation reactions, as a precursor of the second messenger molecule cyclic ADP-ribose, as well as acting as a substrate for bacterial DNA ligases and a group of enzymes called sirtuins that use NAD + to remove acetyl groups from proteins.
Cyclic dinucleotides-second-messenger signaling molecules produced by diverse bacterial species were detected in the cytosol of mammalian cells during intracellular pathogen infection; this leads to activation of TBK1-IRF3 and the downstream production of type I interferon.