987 resultados para PEG 1500
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Alcance y contenido: Copia ms. de fragmentos de varios capitulos de las Cortes celebradas entre 1418 en Valencia y 1510 en Monzón siendo reyes Alfonso V el Magnánimo (1416-1458) y Fernando el Católico (1474-1517).
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Sign.: [ ]4, [asterisco]-2[asterisco]4, 3[asterisco]2, Aa-Zz4
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Sign. : []2, A-Z4, 2A-2Z4, 3A-3D4
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Marca tip. en port
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Tít. tomado de comienzo de texto
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Cancer is a progressive multigenic disorder characterized by defined changes in the transformed phenotype that culminates in metastatic disease. Determining the molecular basis of progression should lead to new opportunities for improved diagnostic and therapeutic modalities. Through the use of subtraction hybridization, a gene associated with transformation progression in virus- and oncogene-transformed rat embryo cells, progression elevated gene-3 (PEG-3), has been cloned. PEG-3 shares significant nucleotide and amino acid sequence homology with the hamster growth arrest and DNA damage-inducible gene gadd34 and a homologous murine gene, MyD116, that is induced during induction of terminal differentiation by interleukin-6 in murine myeloid leukemia cells. PEG-3 expression is elevated in rodent cells displaying a progressed-transformed phenotype and in rodent cells transformed by various oncogenes, including Ha-ras, v-src, mutant type 5 adenovirus (Ad5), and human papilloma virus type 18. The PEG-3 gene is transcriptionally activated in rodent cells, as is gadd34 and MyD116, after treatment with DNA damaging agents, including methyl methanesulfonate and γ-irradiation. In contrast, only PEG-3 is transcriptionally active in rodent cells displaying a progressed phenotype. Although transfection of PEG-3 into normal and Ad5-transformed cells only marginally suppresses colony formation, stable overexpression of PEG-3 in Ad5-transformed rat embryo cells elicits the progression phenotype. These results indicate that PEG-3 is a new member of the gadd and MyD gene family with similar yet distinct properties and this gene may directly contribute to the transformation progression phenotype. Moreover, these studies support the hypothesis that constitutive expression of a DNA damage response may mediate cancer progression.
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Cancer is a progressive disease culminating in acquisition of metastatic potential by a subset of evolving tumor cells. Generation of an adequate blood supply in tumors by production of new blood vessels, angiogenesis, is a defining element in this process. Although extensively investigated, the precise molecular events underlying tumor development, cancer progression, and angiogenesis remain unclear. Subtraction hybridization identified a genetic element, progression elevated gene-3 (PEG-3), whose expression directly correlates with cancer progression and acquisition of oncogenic potential by transformed rodent cells. We presently demonstrate that forced expression of PEG-3 in tumorigenic rodent cells, and in human cancer cells, increases their oncogenic potential in nude mice as reflected by a shorter tumor latency time and the production of larger tumors with increased vascularization. Moreover, inhibiting endogenous PEG-3 expression in progressed rodent cancer cells by stable expression of an antisense expression vector extinguishes the progressed cancer phenotype. Cancer aggressiveness of PEG-3 expressing rodent cells correlates directly with increased RNA transcription, elevated mRNA levels, and augmented secretion of vascular endothelial growth factor (VEGF). Furthermore, transient ectopic expression of PEG-3 transcriptionally activates VEGF in transformed rodent and human cancer cells. Taken together these data demonstrate that PEG-3 is a positive regulator of cancer aggressiveness, a process regulated by augmented VEGF production. These studies also support an association between expression of a single nontransforming cancer progression-inducing gene, PEG-3, and the processes of cancer aggressiveness and angiogenesis. In these contexts, PEG-3 may represent an important target molecule for developing cancer therapeutics and inhibitors of angiogenesis.
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Transformation of normal cloned rat embryo fibroblast (CREF) cells with cellular oncogenes results in acquisition of anchorage-independent growth and oncogenic potential in nude mice. These cellular changes correlate with an induction in the expression of a cancer progression-promoting gene, progression elevated gene-3 (PEG-3). To define the mechanism of activation of PEG-3 as a function of transformation by the Ha-ras and v-raf oncogenes, evaluations of the signaling and transcriptional regulation of the ~2.0 kb promoter region of the PEG-3 gene, PEG-Prom, was undertaken. The full-length and various mutated regions of the PEG-Prom were linked to a luciferase reporter construct and tested for promoter activity in CREF and oncogene-transformed CREF cells. An analysis was also performed using CREF cells doubly transformed with Ha-ras and the Ha-ras specific suppressor gene Krev-1, which inhibits the transformed phenotype in vitro. These assays document an association between expression of the transcription regulator PEA3 and PEG-3. The levels of PEA3 and PEG-3 RNA and proteins are elevated in the oncogenically transformed CREF cells, and reduced in transformation and tumorigenic suppressed Ha-ras/Krev-1 doubly transformed CREF cells. Enhanced tumorigenic behavior, PEG-3 promoter function and PEG-3 expression in Ha-ras transformed cells were all dependent upon increased activity within the mitogen-activated protein kinase (MAPK) pathway. Electrophoretic mobility shift assays and DNase I footprinting experiments indicate that PEA3 binds to sites within the PEG-Prom in transformed rodent cells in an area adjacent to the TATA box in a MAPK-dependent fashion. These findings demonstrate an association between Ha-ras and v-raf transformation of CREF cells with elevated PEA3 and PEG-3 expression, and they implicate MAPK signaling via PEA3 as a signaling cascade involved in activation of the PEG-Prom.
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Recognition of peptides bound to class I major histocompatibility complex (MHC) molecules by specific receptors on T cells regulates the development and activity of the cellular immune system. We have designed and synthesized de novo cyclic peptides that incorporate PEG in the ring structure for binding to class I MHC molecules. The large PEG loops are positioned to extend out of the peptide binding site, thus creating steric effects aimed at preventing the recognition of class I MHC complexes by T-cell receptors. Peptides were synthesized and cyclized on polymer support using high molecular weight symmetrical PEG dicarboxylic acids to link the side chains of lysine residues substituted at positions 4 and 8 in the sequence of the HLA-A2-restricted human T-lymphotrophic virus type I Tax peptide. Cyclic peptides promoted the in vitro folding and assembly of HLA-A2 complexes. Thermal denaturation studies using circular dichroism spectroscopy showed that these complexes are as stable as complexes formed with antigenic peptides.
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Fueron las actuaciones que van de 1500 a 1516 las que hicieron destacar a la diplomacia y el ejército de la Monarquía Hispánica que en estos 16 años consiguieron la total incorporación de Nápoles a la Corona y una muy buena red diplomática y militar en Italia tan efectiva que logran derrotar dos veces a Luis XII de Francia. Baste con leer las palabras que Maquiavelo dedicó a Fernando el Católico en Il Principe en el capítulo XII dedicado a los príncipes que han sabido hacerse estimados. A Maquiavelo no se le ocurre un mejor ejemplo de una mezcla entre príncipe hereditario y príncipe nuevo, dado que hereda el reino de Aragón, pero él se convirtió en rey de España y por su gloria el primer rey de la Cristiandad. Bajo la lupa del embajador florentino, Fernando siempre ha hecho hazañas raras como la conquista de Granada, las guerras de África e Italia o ataques a Francia, y además Fernando el Católico las ha ido encdenando una tras otra de manera que ha conseguido poner los esfuerzos de sus súbditos en estas hazañas, sin dejarles tiempo para la conspiración.Además, la red diplomática y militar de Fernando, en manos de Carlos V y Felipe II, conseguirá, no el equilibrio italiano con el que Fernando soñaba, sino una verdadera hegemonía de la Monarquía Hispánica en la Península Italiana. La Biblioteca Histórica de Marques de Valdecilla es el lugar idóneo en el que desarrollar la exposición dado el fondo bibliográfico que tiene. Uno de los puntos fuertes son las distintas obras que tiene del propio fundador de la Universidad Complutense, el Cardenal Francisco Jiménez de Cisneros, coetáneo a los hechos que queremos exponer. De hecho, es impresionante el ingente número de biografías del propio Cisneros que guarda la biblioteca. Además, fruto del apoyo de la monarquía y de la importancia misma de la Universidad Complutense, tenemos un alto número de historias de varios lugares y personajes. Además, los fondos provenientes del Colegio de los Jesuitas combinan bien con los fondos propios, con lo que se enriquece el resultado final de 60 obras estudiadas.Además, se demuestra el carácter internacional de los fondos, dado que se pueden encontrar obras en francés, italiano y catalán que ayudan a comprender la circulación de textos en diferentes idiomas desde el siglo XVI.
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Las transformaciones padecidas por los musulmanes de Granada a raíz de la conversión masiva de 1499-1500 se reflejan en el cambio antroponímico inicial y su evolución durante el siglo XVI. En este estudio se evalúa la autenticidad de los nombres árabes en los documentos castellanos y se propone una metodología onomástica que abarca dos sistemas diversos (el árabe y el castellano) y que permite un cierto grado de sincretismo. La onomástica comparativa (sincrónica y diacrónica) desde la Edad Media hasta la Moderna, con muestras de otros colectivos permite calibrar el grado de aculturación de los moriscos y descubrir patrones de comportamiento cultural que resultan difícilmente discernibles por otros medios.