https://www.selleckchem.com/products/proxalutamide-gt0918.html A common theme among previously proposed models for network epidemics is the assumption that the propagating object (e.g., a pathogen [in the context of infectious disease propagation] or a piece of information [in the context of information propagation]) is transferred across network nodes without going through any modification or evolutionary adaptations. However, in real-life spreading processes, pathogens often evolve in response to changing environments and medical interventions, and information is often modified by individuals before being forwarded. In this article, we investigate the effects of evolutionary adaptations on spreading processes in complex networks with the aim of 1) revealing the role of evolutionary adaptations on the threshold, probability, and final size of epidemics and 2) exploring the interplay between the structural properties of the network and the evolutionary adaptations of the spreading process.Posttranslational modifications (PTMs) are important physiological means to regulate the activities and structures of central regulatory proteins in health and disease. Small GTPases have been recognized as important molecules that are targeted by PTMs during infections of mammalian cells by bacterial pathogens. The enzymes DrrA/SidM and AnkX from Legionella pneumophila AMPylate and phosphocholinate Rab1b during infection, respectively. Cdc42 is AMPylated by IbpA from Histophilus somni at tyrosine 32 or by VopS from Vibrio parahaemolyticus at threonine 35. These modifications take place in the important regulatory switch I or switch II regions of the GTPases. Since Rab1b and Cdc42 are central regulators of intracellular vesicular trafficking and of the actin cytoskeleton, their modifications by bacterial pathogens have a profound impact on the course of infection. Here, we addressed the biochemical and structural consequences of GTPase AMPylation and phosphocholination. By combinin