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The Global ETD Search service is a free service for researchers
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Networked Digital Library of Theses and Dissertations.
Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
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Showing 41 to 42 of 42 (0.043 seconds)Spelling suggestions: "subject:"neurotrophin"" "subject:"neurotrophins""
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Mecanismes moleculars en el transtorn de la conducta alimentària: estudis en humans i en model murinsMercader Bigas, Josep Maria 11 July 2008 (has links)
Els trastorns de la conducta alimentària (TCA) tenen una etiologia complexa en la que hi intervenen factors de predisposició socioculturals, ambientals i genètics. S'ha aprofundit en les bases moleculars dels TCA mitjançant estudis en pacients i en models murins. S'ha descrit una alteració en la concentració de BDNF en plasma de pacients, una correlació d'aquests nivells amb trets psicopatològics, i una associació de determinats polimorfismes a bulímia nerviosa i als nivells de BDNF en plasma. Un estudi d'associació en vàries poblacions ha demostrat una forta associació de variants del gen NTRK3, amb epistasi amb NGF, a TCA. Un model de sobreexpressió de BDNF confirma el seu paper en la regulació del pes corporal i estableix un possible vincle entre BDNF i la fisiopatologia de les tremolors. La caracterització del ratolí anx/anx suggereix que pot ser un model de la síndrome caquètica que acompanya malalties com el càncer, la SIDA o les malalties autoimmunitàries. / Eating disorders (ED) are complex disorders were environmental, sociocultural and genetic factors are involved. We have improved the knowledge of the genetic basis of ED through studies involving ED patients and murine models. Altered BDNF blood levels have been linked to ED and its related psychopathological traits. In addition several polymorphisms in the BDNF gene have been associated to bulimia nervosa and BDNF plasma levels. A family based association study has shown a strong association of NTRK3 variants to ED which show epistasis with NGF. The generation of an overexpression mouse model for BDNF confirms its role in body weight regulation and establishes a possible link between BDNF and the pathophysiology of tremors. The characterization of the anx/anx mouse model suggests that it may be a good model for the cachexia syndrome that accompanies certain chronic or inflammatory diseases such as cancer, AIDS or autoimmune diseases.
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Micro RNA-Mediated regulation of the full-length and truncated isoforms of human neurotrophic tyrosine kinase receptor type 3 (NTRK 3)Guidi, Mònica 13 January 2009 (has links)
Neurotrophins and their receptors are key molecules in the development of thenervous system. Neurotrophin-3 binds preferentially to its high-affinity receptorNTRK3, which exists in two major isoforms in humans, the full-length kinaseactiveform (150 kDa) and a truncated non-catalytic form (50 kDa). The twovariants show different 3'UTR regions, indicating that they might be differentiallyregulated at the post-transcriptional level. In this work we explore howmicroRNAs take part in the regulation of full-length and truncated NTRK3,demonstrating that the two isoforms are targeted by different sets of microRNAs.We analyze the physiological consequences of the overexpression of some of theregulating microRNAs in human neuroblastoma cells. Finally, we providepreliminary evidence for a possible involvement of miR-124 - a microRNA with noputative target site in either NTRK3 isoform - in the control of the alternativespicing of NTRK3 through the downregulation of the splicing repressor PTBP1. / Las neurotrofinas y sus receptores constituyen una familia de factores crucialespara el desarrollo del sistema nervioso. La neurotrofina 3 ejerce su funciónprincipalmente a través de una unión de gran afinidad al receptor NTRK3, del cualse conocen dos isoformas principales, una larga de 150KDa con actividad de tipotirosina kinasa y una truncada de 50KDa sin dicha actividad. Estas dos isoformasno comparten la misma región 3'UTR, lo que sugiere la existencia de unaregulación postranscripcional diferente. En el presente trabajo se ha exploradocomo los microRNAs intervienen en la regulación de NTRK3, demostrando que lasdos isoformas son reguladas por diferentes miRNAs. Se han analizado lasconsecuencias fisiológicas de la sobrexpresión de dichos microRNAs utilizandocélulas de neuroblastoma. Finalmente, se ha estudiado la posible implicación delmicroRNA miR-124 en el control del splicing alternativo de NTRK3 a través de laregulación de represor de splicing PTBP1.
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