It is often suggested that the Greek tragedians present clinically credible pictures of mental disturbance. https://www.selleckchem.com/products/dzd9008.html For instance, some modern interpreters have compared the process by which Cadmus brings Agave back to sanity in Euripides' Bacchae with modern psychotherapy. But a reading of medical writers' views on the psychological dimension of medicine offers little evidence for believing that these scenes reflect the practices of late fifth-century Athenian doctors, for whom verbal cures are associated with older traditions of non-rational thought, and thus are scorned in favor of more "scientific cures" based on diet or medication. This paper will argue that Athenian tragedians, working from older traditions that advocated verbal cures for some mental ailments, do understand the potential psychological effects that their work can have on audiences, since tragedy requires psychological interaction with its audience in order to be effective. From a close reading of select scenes in Euripidean tragedy, this paper suggests that the experiences of the characters who experience suffering in Euripides' Heracles and Bacchae are analogues of the experiences undergone by the spectators of tragedy at large. Parallels are made between the way that Agave and Heracles are both talked back to sanity by looking upon what has happened, and the way that tragedians make their audiences observe lamentations and meditations that follow the central tragic act, to help them return from the intense emotion provoked, perhaps, by the violence they have seen.The m7G cap marks the 5' end of all eukaryotic mRNAs, but there are also capped ends that map downstream within spliced exons. A portion of the mRNA transcriptome undergoes a cyclical process of decapping and recapping, termed cap homeostasis, which impacts the translation and stability of these mRNAs. Blocking cytoplasmic capping results in the appearance of uncapped 5' ends at native cap sites but also near downstream cap sites. If translation initiates at these sites the products would lack the expected N-terminal sequences, raising the possibility of a link between mRNA recapping and proteome complexity. We performed a shotgun proteomics analysis on cells carrying an inducible inhibitor of cytoplasmic capping. A total of 21 875 tryptic peptides corresponding to 3565 proteins were identified in induced and uninduced cells. Of these, only 29 proteins significantly increased, and 28 proteins significantly decreased, when cytoplasmic capping was inhibited, indicating mRNA recapping has little overall impact on protein expression. In addition, overall peptide coverage per protein did not change significantly when cytoplasmic capping was inhibited. Together with previous work, our findings indicate cap homeostasis functions primarily in gating mRNAs between translating and non-translating states, and not as a source of proteome complexity.Several neurodegenerative diseases of humans and animals are caused by the misfolded prion protein (PrPSc), a self-propagating protein infectious agent that aggregates into oligomeric, fibrillar structures and leads to cell death by incompletely understood mechanisms. Work in multiple biological model systems, from simple baker's yeast to transgenic mouse lines, as well as in vitro studies, has illuminated molecular and cellular modifiers of prion disease. In this review, we focus on intersections between PrP and the proteostasis network, including unfolded protein stress response pathways and roles played by the powerful regulators of protein folding known as protein chaperones. We close with analysis of promising therapeutic avenues for treatment enabled by these studies.Intercalation allows cells to exchange positions in a spatially oriented manner in an array of diverse processes, spanning convergent extension in embryonic gastrulation to the formation of tubular organs. However, given the co-occurrence of cell intercalation and changes in cell shape, it is sometimes difficult to ascertain their respective contribution to morphogenesis. A well-established model to analyse intercalation, particularly in tubular organs, is the Drosophila tracheal system. There, fibroblast growth factor (FGF) signalling at the tip of the dorsal branches generates a 'pulling' force believed to promote cell elongation and cell intercalation, which account for the final branch extension. Here, we used a variety of experimental conditions to study the contribution of cell elongation and cell intercalation to morphogenesis and analysed their mutual requirements. We provide evidence that cell intercalation does not require cell elongation and vice versa. We also show that the two cell behaviours are controlled by independent but simultaneous mechanisms, and that cell elongation is sufficient to account for full extension of the dorsal branch, while cell intercalation has a specific role in setting the diameter of this structure. Thus, rather than viewing changes in cell shape and cell intercalation as just redundant events that add robustness to a given morphogenetic process, we find that they can also act by contributing to different features of tissue architecture.The ubiquitin-proteasome system (UPS) is responsible for the rapid targeting of proteins for degradation at 26S proteasomes and requires the orchestrated action of E1, E2 and E3 enzymes in a well-defined cascade. F-box proteins (FBPs) are substrate-recruiting subunits of Skp1-cullin1-FBP (SCF)-type E3 ubiquitin ligases that determine which proteins are ubiquitinated. To date, around 70 FBPs have been identified in humans and can be subdivided into distinct families, based on the protein-recruiting domains they possess. The FBXL subfamily is defined by the presence of multiple leucine-rich repeat (LRR) protein-binding domains. But how the 22 FBPs of the FBXL family achieve their individual specificities, despite having highly similar structural domains to recruit their substrates, is not clear. Here, we review and explore the FBXL family members in detail highlighting their structural and functional similarities and differences and how they engage their substrates through their LRRs to adopt unique interactomes.