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The mammalian target of rapamycin (mTOR) controls cell growth and size. Amino acids are known to activate TOR, and Rag (Ras-related GTP-binding protein) GTPases have now been found to act as their effectors.
Endothelial barrier function requires the adhesive activity of VE-cadherin and claudin-5, which are key components of adherens and tight endothelial junctions, respectively. Emerging evidence suggests that VE-cadherin controls claudin-5 expression by preventing the nuclear accumulation of FoxO1 and β-catenin, which repress the claudin-5 promoter. This indicates that a crosstalk mechanism operates between these junctional structures.
In endocrine cells, secretion can be rapidly upregulated in response to stimuli without the need for additional synthesis of transport components. A new and unexpected function of KDEL-R as a signalling receptor that senses cargo protein load in the early secretory pathway has been identified.
Cellular senescence, the permanent state of cell-cycle arrest, is emerging as an intrinsic barrier against tumorigenesis and a mechanism contributing to organismal ageing. Unexpected findings now identify multiple secreted inflammatory cytokines, their cognate receptors and positive-feedback loops with corresponding transcription factors, as key mediators of both oncogene-induced and replicative senescence.
Miz1, a Myc-associated transcriptional repressor inhibits cell proliferation. Eilers and colleagues show that the ribosomal protein L23 negatively regulates Miz1 by retaining its activator, nucleophosmin, in the nucleolus.
Namy et al. show that the yeast prion form of the eERF3 translation termination factor boosts antizyme expression, which reduces polyamine synthesis. Changes in polyamine levels account for most of the phenotypic traits conferred by this prion.