1,721,291 research outputs found
When do the expectations of others matter? Experimental evidence on distributional justice and guilt aversion
Full text linkDistributional justice—measured by the proportionality between effort exerted and rewards obtained—and guilt aversion—triggered by not fulfilling others’ expectations—are widely acknowledged fundamental sources of pro-social behavior. We design three experiments to study the relevance of these sources of behavior when considered in interaction. In particular, we investigate whether subjects fulfill others’ expectations also when this could produce inequitable allocations that conflict with distributional justice considerations. Our results confirm that both justice considerations and guilt aversion are important drivers of pro-social behavior, with the former having an overall stronger impact than the latter. Expectations of others are less relevant in environments more likely to nurture equitable outcomes
Two glycosphingolipid sialyltransferases are localized in different sub-Golgi compartments in rat liver
No full textSubcellular biosynthesis and trasport of gangliosides formed from exogenous lactosylceramide in rat liver
No full textPrecursor-product relationship between GM1 and GD1a biosynthesized from exogenous GM2 ganglioside in rat liver
No full textThe demonstration of a precursor-product relationship in the course of GM1 and GD1a biosynthesis is described in the present paper. We injected rats with GM2 gangliosides [GalNAc beta 1----4(NeuAc alpha 2----3)Gal beta 1----4Glc beta 1----1'Cer] of brain origin, which were isotopically radiolabeled on the GalNAc ([GalNAc-3H]GM2) or sphingosine ([Sph-3H]GM2) residue. We then compared the time-courses of GM1 and GD1a biosynthesis in the liver after the administration of each radiolabeled GM2 derivative. After the administration of [GalNAc-3H]GM2, GM1, and GD1a were both present as doublets, that could be easily resolved on TLC. The lower spot of each doublet was identified as a species having the typical rat brain ceramide moiety and represented gangliosides formed through direct glycosylation of the injected GM2. The upper spot of each doublet was identified as a species having the typical rat liver ceramide moiety and represented gangliosides formed through recycling of the [3H]GalNAc residue, released during ganglioside catabolism. After the administration of [Sph-3H]GM2, only ganglioside with the rat brain ceramide moiety were found, that represented the sum of ganglioside formed through direct glycosylation and those formed through recycling of some sphingosine-containing fragments. In each case, the time-course of GM1 and GD1a biosynthesis exhibited a precursor-product relationship. The curve obtained from the direct glycosylation showed a timing delay with respect to those obtained from recycling of GM2 fragments. These results are consistent with the hypothesis that the sequential addition of activated sugars to a sphingolipid precursor is a dissociative process, catalyzed by physically independent enzymatic activities
Familial Alzheimerâ€TMs Disease presenilin mutants reduce calcium levels of intracellular stores. A critical revaluation of the “calcium overload†hypothesis
No full textBackground: Presenilin-1 and -2 (PS1 and PS2) mutations, the major cause of Familial Alzheimer’s Disease (FAD), have been causally implicated in the pathogenesis of neuronal cell death through a perturbation of cellular Ca2+ homeostasis. We have recently shown that, at variance with previous suggestions obtained in cells expressing other FAD-linked PS mutations, PS2-M239I and PS2-T122R cause a reduction and not an increase in cytosolic Ca2+ rises induced by Ca2+ release from stores (1,2). Objective(s): In this study we aim at investigating whether other FAD-linked PS mutations induce a similar dysregulation of Ca2+ homeostasis. Methods: Different cell models have been used: human fibroblasts from controls and FAD patients, cell lines (SH-SY5Y, HeLa, HEK293, MEFs) and rat primary neurons expressing a number of PS mutations, e.g. P117L, M146L, L286V, and A246E in PS1 and M239I, T122R, and N141I in PS2. The effects of FAD-linked PS mutations on cytosolic Ca2+ changes have been monitored either by using fura-2 or recombinant cytosolic aequorin as the probe. Results: Independently of the cell model or the employed probe, the cytosolic Ca2+ increases, caused by agonist stimulation or full store depletion by drug treatment, were reduced or unchanged in cells expressing the PS mutations. Using aequorins, targeted to the endoplasmic reticulum or the Golgi apparatus, we here show that FAD-linked PS mutants lower the Ca2+ content of intracellular stores. The phenomenon was most prominent in cells expressing PS2 mutants, and was observed also in cells expressing the non-pathogenic, “loss-of-function” PS2-D366A mutation. Conclusions: Taken as a whole, our findings, while confirming the capability of presenilins to modify Ca2+ homeostasis, suggest a re-evaluation of the “Ca2+ hypothesis” in AD and a new working hypothesis is presented.
1. Zatti G, Ghidoni R, Barbiero L, Binetti G, Pozzan T, Fasolato C, Pizzo P. (2004). Neurobiology of disease, 15, 269-278.
2. Giacomello M, Barbiero L, Zatti G, Squitti R, Binetti G, Pozzan T, Fasolato C, Ghidoni R, Pizzo P. (2005). Neurobiology of disease, 18, 638-648
Topography of glycosyltransferases involved in the initial glycosylation of gangliosides
No full textSub-Golgi distribution in rat liver of CMP-NeuAc: GM3- and CMP-NeuAc: GT1b alpha2-8 sialyltransferases and comparison with the distribution the other glycosyltransferase activities involved in ganglioside biosynthesis
No full textLocalization in the Golgi apparatus of rat liver UDP-Gal: glucosylceramide beta1-4 galactosyltransferase
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