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51.
Pierre-Olivier Roy Louise Deschênes Manuele Margni 《The International Journal of Life Cycle Assessment》2014,19(4):882-890
Purpose
Characterization factors (CFs) quantifying the potential impact of acidifying emissions on inland aquatic environments in life cycle assessment are typically available on a generic level. The lack of spatial differentiation may weaken the relevance of generic CFs since it was shown that regional impact categories such as aquatic acidification were influenced by the surroundings of the emission location. This paper presents a novel approach for the development of spatially differentiated CFs at a global scale for the aquatic acidification impact category.Methods
CFs were defined as the change in relative decrease of lake fish species richness due to a change in acidifying chemicals emissions. The characterization model includes the modelling steps linking emission to atmospheric acid deposition (atmospheric fate factor) change, which lead to lake H+ concentration (receiving environment fate factor) change and a decrease in relative fish species richness (effect factor). We also evaluated the significance of each factor (i.e. atmospheric fate, receiving environment fate and effects) to the overall CFs spatial variability and parameter uncertainty.Results and discussion
The highest CFs were found for emissions occurring in Canada, Scandinavia and the northern central Asia because of the extensive lake areas in these regions (lake areas being one of the parameters of the CFs; the bigger the lake areas, the higher the CFs). The CFs’ spatial variability ranged over 5, 6 and 8 orders of magnitude for NOx, SO2 and NH3 emissions, respectively. We found that the aquatic receiving environment fate factor is the dominant contributor to the overall spatial variability of the CFs, while the effect factors contributed to 98 % of the total parameter uncertainty.Conclusions
The resulting characterization model and factors enable a consistent evaluation of spatially explicit acidifying emissions impacts at the global scale. 相似文献52.
Stéphane Vassilopoulos Christel Gentil Jeanne Lainé Pierre-Olivier Buclez Agathe Franck Arnaud Ferry Guillaume Précigout Robyn Roth John E. Heuser Frances M. Brodsky Luis Garcia Gisèle Bonne Thomas Voit France Piétri-Rouxel Marc Bitoun 《The Journal of cell biology》2014,204(3):377-393
Export of newly synthesized G protein–coupled receptors (GPCRs) remains poorly characterized. We show in this paper that lipocalin-type prostaglandin D2 (PGD2) synthase (L-PGDS) interacts intracellularly with the GPCR DP1 in an agonist-independent manner. L-PGDS promotes cell surface expression of DP1, but not of other GPCRs, in HEK293 and HeLa cells, independent of L-PGDS enzyme activity. In addition, formation of a DP1–Hsp90 complex necessary for DP1 export to the cell surface is dependent on the interaction between L-PGDS and the C-terminal MEEVD residues of Hsp90. Surprisingly, PGD2 synthesis by L-PGDS is promoted by coexpression of DP1, suggesting a possible intracrine/autocrine signaling mechanism. In this regard, L-PGDS increases the formation of a DP1–ERK1/2 complex and increases DP1-mediated ERK1/2 signaling. Our findings define a novel cooperative mechanism in which a GPCR (DP1) promotes the activity of the enzyme (L-PGDS) that produces its agonist (PGD2) and in which this enzyme in turn acts as a cofactor (of Hsp90) to promote export and agonist-dependent activity of the receptor. 相似文献
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V.K. Chaithanya Ponnaluri Pierre-Olivier Estève Cristian I. Ruse Sriharsa Pradhan 《Journal of molecular biology》2018,430(14):2051-2065
DNA (cytosine-5) methyltransferase 1 (DNMT1) is essential for mammalian development and maintenance of DNA methylation following DNA replication in cells. The DNA methylation process generates S-adenosyl-l-homocysteine, a strong inhibitor of DNMT1. Here we report that S-adenosylhomocysteine hydrolase (SAHH/AHCY), the only mammalian enzyme capable of hydrolyzing S-adenosyl-l-homocysteine binds to DNMT1 during DNA replication. SAHH enhances DNMT1 activity in vitro, and its overexpression in mammalian cells led to hypermethylation of the genome, whereas its inhibition by adenosine periodate or siRNA-mediated knockdown resulted in hypomethylation of the genome. Hypermethylation was consistent in both gene bodies and repetitive DNA elements leading to aberrant gene regulation. Cells overexpressing SAHH specifically up-regulated metabolic pathway genes and down-regulated PPAR and MAPK signaling pathways genes. Therefore, we suggest that alteration of SAHH level affects global DNA methylation levels and gene expression. 相似文献
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Francesca Santostefano Dany Garant Patrick Bergeron Pierre-Olivier Montiglio Denis Réale 《Evolution; international journal of organic evolution》2020,74(1):89-102
Through social interactions, phenotypes of conspecifics can affect an individual's fitness, resulting in social selection. Social selection is assumed to represent a strong and dynamic evolutionary force that can act with or in opposition to natural selection. Few studies, however, have estimated social selection and its contribution to total selection in the wild. We estimated natural and social selection gradients on exploration, docility, and body mass, and their contribution to selection differentials, in a wild eastern chipmunk population (Tamias striatus). We applied trait-based multiple regression models derived from classical phenotypic selection analyses, which allowed us to include several social partners (i.e., neighbors). We detected social selection gradients on female docility and male body mass, indicating that female with docile neighbors and males with large neighbors had lower fitness. In both sexes, social selection gradients varied with the season. However, we found no phenotypic assortment or disassortment for the studied traits. Social selection gradients, therefore, did not contribute to total selection differentials, and natural selection alone could drive phenotypic changes. Evaluating the factors that drive the evolution of the covariance between interacting phenotypes is necessary to understand the role of social selection as an evolutionary force. 相似文献
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Roy Pierre-Olivier Bulle Cécile Deschênes Louise 《The International Journal of Life Cycle Assessment》2019,24(1):93-103
The International Journal of Life Cycle Assessment - Metals have often been identified as the main contributors to (eco)toxicological impacts in life cycle assessment (LCA) studies. Indeed,... 相似文献
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Endothelin-1 (ET-1) and angiotensin II (AngII), two potent vasoactive peptides involved in the regulation of cardiovascular homeostasis, also induce mitogenic and pro-angiogenic responses in vitro and in vivo. Both peptides are produced by cleavage of inactive precursors by metalloproteases (endothelin-converting enzyme and angiotensin-converting enzyme, respectively) and activate two subtypes of membrane receptors (ETA-R and ETB-R for ET-1, AT1R and AT2R for AngII) that all belong to the superfamily of G-protein coupled receptors. There is increasing evidence that ETA-R, ETB-R and AT1R are expressed in a variety of cancer cells and tissues, and may play a role on tumor growth, angiogenesis and invasion in vivo. This review summarizes the similarities and differences between the ET-1 and AngII systems with regard to their reported effects on various aspects of cancer. In addition to being expressed on vascular endothelium, ET-1 and AngII receptors participate in tumor angiogenesis through the production of the angiogenic factor VEGF. Furthermore, recent clinical studies indicate that a selective ETA-R antagonist has beneficial effects in prostate cancer, suggesting that a similar approach using ETB-R and AT1R blockers might be envisioned. Experimental data presented here suggest that a combined therapy targeting both ET-1 and AngII systems may prove valuable for future treatments of highly angiogenic tumors. 相似文献
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Chloé Journo Josina Filipe Frédégonde About Sébastien A. Chevalier Philippe V. Afonso John N. Brady David Flynn Frédéric Tangy Alain Isra?l Pierre-Olivier Vidalain Renaud Mahieux Robert Weil 《PLoS pathogens》2009,5(7)
Nuclear factor (NF)-κB is a major survival pathway engaged by the Human T-Lymphotropic Virus type 1 (HTLV-1) Tax protein. Tax1 activation of NF-κB occurs predominantly in the cytoplasm, where Tax1 binds NF-κB Essential Modulator (NEMO/IKKγ) and triggers the activation of IκB kinases. Several independent studies have shown that Tax1-mediated NF-κB activation is dependent on Tax1 ubiquitination. Here, we identify by co-immunoprecipitation assays NEMO-Related Protein (NRP/Optineurin) as a binding partner for Tax1 in HTLV-1 infected and Tax1/NRP co-expressing cells. Immunofluorescence studies reveal that Tax1, NRP and NEMO colocalize in Golgi-associated structures. The interaction between Tax1 and NRP requires the ubiquitin-binding activity of NRP and the ubiquitination sites of Tax1. In addition, we observe that NRP increases the ubiquitination of Tax1 along with Tax1-dependent NF-κB signaling. Surprisingly, we find that in addition to Tax1, NRP interacts cooperatively with the Tax1 binding protein TAX1BP1, and that NRP and TAX1BP1 cooperate to modulate Tax1 ubiquitination and NF-κB activation. Our data strongly suggest for the first time that NRP is a critical adaptor that regulates the assembly of TAX1BP1 and post-translationally modified forms of Tax1, leading to sustained NF-κB activation. 相似文献