453 resultados para Chaîne invariante p35
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Anna Schapire
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Siegfried Abeles
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Siegfried Abeles
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Most poxviruses, including variola, the causative agent of smallpox, express a secreted protein of 35 kDa, vCCI, which binds CC-chemokines with high affinity. This viral protein competes with the host cellular CC-chemokine receptors (CCRs), reducing inflammation and interfering with the host immune response. Such proteins or derivatives may have therapeutic uses as anti-inflammatory agents. We have determined the crystal structure to 1.85-Å resolution of vCCI from cowpox virus, the prototype of this poxvirus virulence factor. The molecule is a β-sandwich of topology not previously described. A patch of conserved residues on the exposed face of a β-sheet that is strongly negatively charged might have a role in binding of CC-chemokines, which are positively charged.
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The Epstein–Barr virus-induced gene 3 (EBI3) is a novel soluble hematopoietin component related to the p40 subunit of interleukin 12 (IL-12). When EBI3 was expressed in cells, it accumulated in the endoplasmic reticulum and associated with the molecular chaperone calnexin, indicating that subsequent processing and secretion might be dependent on association with a second subunit. Coimmunoprecipitations from lysates and culture media of cells transfected with expression vectors for EBI3 and/or the p35 subunit of IL-12 now reveal a specific association of EBI3 with p35. Coexpression of EBI3 and p35 mutually facilitates their secretion. Most importantly, a large fraction of p35 in extracts of the trophoblast component of a human full-term normal placenta specifically coimmunoprecipitated with EBI3, indicating that EBI3 is in a heterodimer with p35, in vivo. Because EBI3 is expressed in EBV-transformed B lymphocytes, tonsil, spleen, and placental trophoblasts, the EBI3/p35 heterodimer is likely to be an important immunomodulator.
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Cyclin-dependent kinase (Cdk) 5 is a unique member of the Cdk family, because Cdk5 kinase activity is detected only in the nervous tissue. Two neuron-specific activating subunits of Cdk5, p35 and p39, have been identified. Overlapping expression pattern of these isoforms in the embryonic mouse brain and the significant residual Cdk5 kinase activity in brain homogenate of the p35−/− mice indicate the redundant functions of the Cdk5 activators in vivo. Severe neuronal migration defects in p35−/−Cdk5 +/− mice further support the idea that the redundant expression of the Cdk5 activators may cause a milder phenotype in p35−/− mice compared with Cdk5−/− mice. Mutant mice lacking either Cdk5 or p35 exhibit certain similarities with Reelin/Dab1-mutant mice in the disorganization of cortical laminar structure in the brain. To elucidate the relationship between Cdk5/p35 and Reelin/Dab1 signaling, we generated mouse lines that have combined defects of these genes. The addition of heterozygosity of either Dab1 or Reelin mutation to p35−/− causes the extensive migration defects of cortical neurons in the cerebellum. In the double-null mice of p35 and either Dab1 or Reelin, additional migration defects occur in the Purkinje cells in the cerebellum and in the pyramidal neurons in the hippocampus. These additional defects in neuronal migration in mice lacking both Cdk5/p35 and Reelin/Dab1 indicate that Cdk5/p35 may contribute synergistically to the positioning of the cortical neurons in the developing mouse brain.
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Cell cycle withdrawal in postmitotic cells involves cyclin-dependent kinase (Cdk) inhibitors that repress cell cycle Cdk activity. During mouse neurogenesis, cortical postmitotic neurons are shown here to accumulate high levels of the p27 Cdk inhibitor compared with their progenitor neuroblasts. Elevated p27 levels in staged embryo brain extracts correlate with p27 binding to Cdk2, and Cdk inactivation. Yet, Cdk5, which is associated with the noncyclin activator p35 in neurons, remains active in the presence of high p27 levels. Both in vitro and in vivo, p27 and related inhibitors can recognize a cyclin D-Cdk5 complex but not a p35-Cdk5 complex. The results indicate that the choice of activator determines the susceptibility of Cdk5 to p27 and related Cdk inhibitors, and thus its ability to act in postmitotic cells.
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Este trabalho aborda o problema de casamento entre duas imagens. Casamento de imagens pode ser do tipo casamento de modelos (template matching) ou casamento de pontos-chaves (keypoint matching). Estes algoritmos localizam uma região da primeira imagem numa segunda imagem. Nosso grupo desenvolveu dois algoritmos de casamento de modelos invariante por rotação, escala e translação denominados Ciratefi (Circula, radial and template matchings filter) e Forapro (Fourier coefficients of radial and circular projection). As características positivas destes algoritmos são a invariância a mudanças de brilho/contraste e robustez a padrões repetitivos. Na primeira parte desta tese, tornamos Ciratefi invariante a transformações afins, obtendo Aciratefi (Affine-ciratefi). Construímos um banco de imagens para comparar este algoritmo com Asift (Affine-scale invariant feature transform) e Aforapro (Affine-forapro). Asift é considerado atualmente o melhor algoritmo de casamento de imagens invariante afim, e Aforapro foi proposto em nossa dissertação de mestrado. Nossos resultados sugerem que Aciratefi supera Asift na presença combinada de padrões repetitivos, mudanças de brilho/contraste e mudanças de pontos de vista. Na segunda parte desta tese, construímos um algoritmo para filtrar casamentos de pontos-chaves, baseado num conceito que denominamos de coerência geométrica. Aplicamos esta filtragem no bem-conhecido algoritmo Sift (scale invariant feature transform), base do Asift. Avaliamos a nossa proposta no banco de imagens de Mikolajczyk. As taxas de erro obtidas são significativamente menores que as do Sift original.
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Mode of access: Internet.
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"Plantes," pp. 297-328.
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"Extrait du Bulletin de la Société d'histoire naturelle d'Autun, tome 7. (année 1895)"
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"Als anhang zur Geschichte des osmanischen reichs." "Türkische quellen," p. 7-11.
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Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.
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Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.
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Ce mémoire s'intéresse à la réception critique de Né à Québec, première œuvre d'Alain Grandbois et aux relectures de ce récit à travers le temps. Cette étude a pour point de départ le paradoxe entre le futur prometteur de l'œuvre que laissait augurer la réception initiale et le rôle bien secondaire que joue désormais Né à Québec dans l'histoire de la littérature québécoise. Le mémoire est divisé en trois chapitres structurés chronologiquement et couvre la réception de l'œuvre de sa publication en 1933 jusqu'à nos jours. Le premier chapitre se penche sur le contexte de réception initial ainsi que sur l'élaboration d'un discours critique dominant sur Né à Québec. Cette partie de l'étude a aussi pour but de rappeler les conclusions de Marcel Fortin sur la réception immédiate de l'œuvre en question telles que décrites dans son ouvrage Histoire d'une célébration, publié il y a maintenant plus de vingt ans. Ce rappel est primordial afin de bien comprendre comment la pensée critique a évolué au-delà de la décennie 1930. À noter que l'analyse présente dans ce mémoire offre une perspective différente que celle de Fortin sur les commentaires de cette période puisqu'elle s'organise autour de concepts théoriques nouveaux, en particulier la notion de stéréotype telle que définie par Jean-Louis Dufays. Les deux autres chapitres traitent de textes critiques sur Né à Québec qui n'ont jamais dans le passé été directement le sujet d'une étude de réception. Tout au long de cette étude, le discours sur l'œuvre de Grandbois est décrit, analysé et comparé afin de comprendre comment ce récit historique en est venu à être aujourd'hui délaissé par le public et les littérateurs du Québec et d'ailleurs.