146 research outputs found

    Diagnóstico de posicionamiento de la Facultad de Ciencias Económicas de la Universidad Nacional de la Patagonia San Juan Bosco

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    En el presente trabajo se muestran los resultados de una investigación que incluye la opinión de actores significativos para determinar el posicionamiento de la Facultad de Ciencias Económicas de la Universidad pública local (FCE - UNPSJB).Se utilizaron técnicas estadísticas de escalado multidimensional, principalmente los mapeados preceptuales, que permiten representar en un diagrama las percepciones de los encuestados en cuanto la posición lograda por la Facultad.Los resultados muestran una situación favorable a la organización respecto de su posicionamiento frente otras instituciones educativas, consideradas en situación de competencia en el Valle Inferior del Río Chubut y Puerto Madryn. Esta zona es la considerada en el proyecto de Investigación, en el que se enmarca el estudio de diagnóstico efectuado. A partir del presente diagnóstico, es menester efectuar un análisis pormenorizado de los factores críticos que surgen de la investigación, utilizando herramientas como las Matrices F.O.D.A., B.C.G. y G.E, para diseñar las estrategias adecuadas de refuerzo del lugar que ocupa la organización en la mente de los potenciales alumnos, para que el posicionamiento diagnosticado se traduzca en efectivos incrementos de matrícula

    Myosin VI small insert isoform maintains exocytosis by tethering secretory granules to the cortical actin.

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    Before undergoing neuroexocytosis, secretory granules (SGs) are mobilized and tethered to the cortical actin network by an unknown mechanism. Using an SG pull-down assay and mass spectrometry, we found that myosin VI was recruited to SGs in a Ca(2+)-dependent manner. Interfering with myosin VI function in PC12 cells reduced the density of SGs near the plasma membrane without affecting their biogenesis. Myosin VI knockdown selectively impaired a late phase of exocytosis, consistent with a replenishment defect. This exocytic defect was selectively rescued by expression of the myosin VI small insert (SI) isoform, which efficiently tethered SGs to the cortical actin network. These myosin VI SI-specific effects were prevented by deletion of a c-Src kinase phosphorylation DYD motif, identified in silico. Myosin VI SI thus recruits SGs to the cortical actin network, potentially via c-Src phosphorylation, thereby maintaining an active pool of SGs near the plasma membrane

    Myosin VI in PC12 cells plays important roles in cell migration and proliferation but not in catecholamine secretion

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    Myosin VI (MVI) is the only known myosin walking towards minus end of actin filaments and is believed to play distinct role(s) than other myosins. We addressed a role of this unique motor in secretory PC12 cells, derived from rat adrenal medulla pheochromocytoma using cell lines with reduced MVI synthesis (produced by means of siRNA). Decrease of MVI expression caused severe changes in cell size and morphology, and profound defects in actin cytoskeleton organization and Golgi structure. Also, significant inhibition of cell migration as well as cell proliferation was observed. Flow cytometric analysis revealed that MVI-deficient cells were arrested in G0/G1 phase of the cell cycle but did not undergo increased senescence as compared with control cells. Also, neither polyploidy nor aneuploidy were detected. Surprisingly, no significant effect on noradrenaline secretion was observed. These data indicate that in PC12 cells MVI is involved in cell migration and proliferation but is not crucial for stimulation-dependent catecholamine release

    Morphological docking of secretory vesicles

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    Calcium-dependent secretion of neurotransmitters and hormones is essential for brain function and neuroendocrine-signaling. Prior to exocytosis, neurotransmitter-containing vesicles dock to the target membrane. In electron micrographs of neurons and neuroendocrine cells, like chromaffin cells many synaptic vesicles (SVs) and large dense-core vesicles (LDCVs) are docked. For many years the molecular identity of the morphologically docked state was unknown. Recently, we resolved the minimal docking machinery in adrenal medullary chromaffin cells using embryonic mouse model systems together with electron-microscopic analyses and also found that docking is controlled by the sub-membrane filamentous (F-)actin. Currently it is unclear if the same docking machinery operates in synapses. Here, I will review our docking assay that led to the identification of the LDCV docking machinery in chromaffin cells and also discuss whether identical docking proteins are required for SV docking in synapses
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