Le Musée de l'histoire de l'immigration à Paris: une collection et un musée en devenir

Globalization and the emergence of political issues in the European Union have propelled the topic of immigration into the center of the current political climate. In this contemporary context, museums that are focused on immigration are gaining more importance due to the impetus for preserving and providing visibility for the heritage of immigrants. In Paris during October 2007 the Cité nationale de l'Histoire de l'Immigration (CNHI) opened its doors but in 2013 it changed its name to Musée de l'histoire de l'immigration (MHI). The museum presents a historical and cultural approach to immigration as well as displaying contemporary works of art that deal with the theme of immigration. In this paper we will analyze how this museum is an attempt to integrate the History of immigration as a national heritage.Com a globalização e o surgimento da Comunidade Europeia, a questão das migrações se apresenta no centro das preocupações políticas mundiais contemporâneas. E nesse contexto histórico de países de imigração ou de emigração organizam-se os museus de estudos das migrações que pertencem à categoria dos museus de história e de sociedade. Em outubro de 2007, é criada, em Paris, a Cité nationale de l'Histoire de l'Immigration (CNHI) que desde 2013 passou a se chamar Musée de l'histoire de l'immigration (MHI): um museu que apresenta ao público uma abordagem histórica e cultural da imigração assim como obras de arte contemporânea que tratam do tema. Neste artigo, bucaremos compreender como este museu constitui uma tentativa de reconhecimento do patrimônio da imigração como um patrimônio nacional.Avec la mondialisation et l'émergence de nouvelles politiques d'immigration dans la Communauté Européenne, la question des migrations est centrale dans le monde politique d'aujourd'hui. C'est dans ce contexte historique de pays d'immigration ou d'émigration que se met en place et s'organise l'étude des musées d'immigration qui appartiennent à la catégorie des musées d'histoire et de société. En France, la Cité nationale de l'Histoire de l'Immigration, qui a ouvert ses portes en octobre 2007, depuis 2013 Musée de l'histoire de l'immigration (MHI), se distingue, dans ce contexte mondial, par l'originalité de son projet et les discussions qu'il suscite dans divers domaines (aussi bien dans le milieu académique que dans les réseaux d'associations qui s'occupent des immigrés en France). Le musée présente au public une approche historique et culturelle de l'immigration ainsi que des œuvres d'art contemporain sur ce sujet. Dans cet article, on s'interrogera sur comment ce musée constitue une tentative de reconnaître le patrimoine de l'immigration comme un patrimoine national

Discours de François Hollande

Madame la Ministre,Monsieur l'Administrateur,Mesdames et Messieurs les Professeurs, Je ne sais pas lequel de Serge Haroche ou de moi-même est le plus impressionné. Lui de me recevoir ici au Collège de France, dont je suis, par les fonctions que j'exerce, le protecteur ; et moi-même, venant ici dans cet amphithéâtre où tant de personnages illustres ont pu diffuser la connaissance et le savoir. Il n'est sans doute pas de plus grand honneur pour un pays que de voir l'un de ses ressortissants rec..

Au stade, on n'est jamais seul : Conversation avec François Hollande

Des souvenirs du stade Robert Diochon de Rouen à la préparation de l'Euro 2016 et la candidature de Paris à l'organisation des Jeux olympiques : conversation sportive avec le président de la République

L'écologie des mondes : paroles d'ici et d'ailleurs sur le climat et l'environnement/ Ecology of our worlds : views on climate and the environment

International audienc

Cells retrovirally transfected with fibroblast growth factor-2 isoforms exhibit altered adenylate cyclase activity and G-protein functionality

Basic fibroblast growth factor (FGF-2) is synthesized as different molecular mass isoforms all lacking the signal-peptide sequence. The high molecular-mass isoforms (21-24 kDa) possess a signal sequence directing their nuclear translocation. The role of each isoform is still poorly understood, however, modifications in intracellular signalling pathways could explain some effects of these peptides. In order to evaluate the role of FGF-2 isoforms on the adenylate cyclase (AC) signalling pathway, we retrovirally infected a rat pancreatic cell line (AR4-2J) with point-mutated FGF-2 cDNAs, allowing the expression of the 18 (A5 cells) or 22.5 kDa isoform (A3 cells) at a low level. In membrane preparations of A3 cells, unscheduled expression of the 22.5 kDa FGF-2 isoform induced a 2-fold decrease in both basal and forskolin-stimulated AC activity. Studies carried out on intact cells also showed decreased accumulation of cAMP in A3 cells in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. Both FGF-2 peptides also induced functional modifications of G-proteins without affecting their levels. The 22.5 kDa peptide led to enhanced ADP-ribosylation of both α(s)-subunits in vitro, whereas the expression of the low molecular-mass 18 kDa peptide resulted in a 2-fold increase in α(i2) and α0 ADP-ribosylations. Furthermore, control CAT cells (AR4-2J cells transfected with the retrovirus containing the chloramphenicol acetyltransferase gene) and A5 cells were growth-inhibited by 8-Br-cAMP, in contrast to A3 cells. These data provide evidence that the expression of FGF-2 peptides could play a role in cell functions by modifying the AC signalling pathway. FGF-2 peptides are able to modulate both AC activity and the regulatory G-proteins. Finally FGF-2 expression may interfere with cAMP-regulated cell proliferation.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

The Wnt Target Jagged-1 Mediates the Activation of Notch Signaling by Progastrin in Human Colorectal Cancer Cells

International audienceThe Wnt and Notch signaling pathways are both abnormally activated in colorectal cancer (CRC). We recently showed that progastrin depletion inhibited Wnt signaling and increased goblet cell differentiation of CRC cells. Here, we show that progastrin down-regulation restores the expression by CRC cells of the early secretory lineage marker Math-1/Hath-1 due to an inhibition of Notch signaling. This effect is mediated by a decreased transcription of the Notch ligand Jagged-1, downstream of beta-catenin/Tcf-4. Accordingly, recombinant progastrin sequentially activated the transcription of Wnt and Notch target genes in progastrin-depleted cells. In addition, restoration of Jagged-1 levels in these cells is sufficient to activate Tcf-4 activity, demonstrating the occurrence of a feedback regulation from Notch toward Wnt signaling. These results suggest that progastrin could be instrumental in maintaining the concomitant activation of Wnt and Notch pathways in CRC cells, further highlighting the interest of progastrin targeting for the clinical management of CRC

SLAP displays tumour suppressor functions in colorectal cancer via destabilization of the SRC substrate EPHA2

International audienceThe adaptor SLAP is a negative regulator of receptor signalling in immune cells but its role in human cancer is ill defined. Here we report that SLAP is abundantly expressed in healthy epithelial intestine but strongly downregulated in 50% of colorectal cancer. SLAP overexpression suppresses cell tumorigenicity and invasiveness while SLAP silencing enhances these transforming properties. Mechanistically, SLAP controls SRC/EPHA2/AKT signalling via destabilization of the SRC substrate and receptor tyrosine kinase EPHA2. This activity is independent from CBL but requires SLAP SH3 interaction with the ubiquitination factor UBE4A and SLAP SH2 interaction with pTyr594-EPHA2. SRC phosphorylates EPHA2 on Tyr594, thus creating a feedback loop that promotes EPHA2 destruction and thereby self-regulates its transforming potential. SLAP silencing enhances SRC oncogenicity and sensitizes colorectal tumour cells to SRC inhibitors. Collectively, these data establish a tumour-suppressive role for SLAP in colorectal cancer and a mechanism of SRC oncogenic induction through stabilization of its cognate substrates

Phosphatidylethanol Accumulation Promotes Intestinal Hyperplasia by Inducing ZONAB-Mediated Cell Density Increase in Response to Chronic Ethanol Exposure

International audienceChronic alcohol consumption is associated with increased risk of gastrointestinal cancer. High concentrations of ethanol trigger mucosal hyperregeneration, disrupt cell adhesion, and increase the sensitivity to carcinogens. Most of these effects are thought to be mediated by acetaldehyde, a genotoxic metabolite produced from ethanol by alcohol dehydrogenases. Here, we studied the role of low ethanol concentrations, more likely to mimic those found in the intestine in vivo, and used intestinal cells lacking alcohol dehydrogenase to identify the acetaldehyde-independent biological effects of ethanol. Under these conditions, ethanol did not stimulate the proliferation of nonconfluent cells, but significantly increased maximal cell density. Incorporation of phosphatidylethanol, produced from ethanol by phospholipase D, was instrumental to this effect. Phosphatidylethanol accumulation induced claudin-1 endocytosis and disrupted the claudin-1/ZO-1 association. The resulting nuclear translocation of ZONAB was shown to mediate the cell density increase in ethanol-treated cells. In vivo, incorporation of phosphatidylethanol and nuclear translocation of ZONAB correlated with increased proliferation in the colonic epithelium of ethanol-fed mice and in adenomas of chronic alcoholics. Our results show that phosphatidylethanol accumulation after chronic ethanol exposure disrupts signals that normally restrict proliferation in highly confluent intestinal cells, thus facilitating abnormal intestinal cell proliferation