{"id":10428,"date":"1996-01-01T00:00:00","date_gmt":"1996-01-01T00:00:00","guid":{"rendered":"https:\/\/www.deberes.net\/tesis\/1996\/01\/01\/regulacion-de-la-prolactina-por-el-tgf-beta1\/"},"modified":"1996-01-01T00:00:00","modified_gmt":"1996-01-01T00:00:00","slug":"regulacion-de-la-prolactina-por-el-tgf-beta1","status":"publish","type":"post","link":"https:\/\/www.deberes.net\/tesis\/ciencias-medicas\/regulacion-de-la-prolactina-por-el-tgf-beta1\/","title":{"rendered":"Regulacion de la prolactina por el tgf-beta1."},"content":{"rendered":"<h2>Tesis doctoral de <strong> Raquel Coya Guerrero <\/strong><\/h2>\n<p>El objetivo de este trabajo ha sido estudiar el papel regulador del tgf-beta1 sobre la sintesis y secrecion de prl asi como conocer su mecanismo de accion intracelular.  los resultados obtenidos demostraron un papel inhibidor del tgf-beta1 sobre la secrecion de prl en cultivos primarios de celulas hipofisarias de rata. El tgf-beta1 inhibio la secrecion basal de prl (de forma dosis y tiempo dependiente) asi como la respuesta a diversos estimulos (trh, forskolina, a23187, (bu) 2ampc). Este efecto fue independiente del sexo. El tgf- beta1 no inhibio la secrecion de otras hormonas hipofisarias y su accion no fue imitada por otros factores de crecimiento.  el tgf-beta1 mostro efectos aditivos con la somatostatina y no con la dopamina. El tgf-beta1 no modifico la fosforilacion de proteinas como la erk-2 activada por la trh. El tgf-beta1 esta asociado, al menos de forma parcial, a una proteina g sensible a la toxina pertussis.  el tgf-beta1 fue capaz de inhibir tambien la expresion del arnm para prl. Este efecto se mostro como tiempo dependiente.  estos resultados no se reprodujeron al utilizar la linea celular gh3 en los estudios.  en esta linea celular el tgf-beta1 si fue capaz de inhibir la proliferacion celular.<\/p>\n<p>&nbsp;<\/p>\n<h3>Datos acad\u00e9micos de la tesis doctoral \u00ab<strong>Regulacion de la prolactina por el tgf-beta1.<\/strong>\u00ab<\/h3>\n<ul>\n<li><strong>T\u00edtulo de la tesis:<\/strong>\u00a0 Regulacion de la prolactina por el tgf-beta1. <\/li>\n<li><strong>Autor:<\/strong>\u00a0 Raquel Coya Guerrero <\/li>\n<li><strong>Universidad:<\/strong>\u00a0 Santiago de compostela<\/li>\n<li><strong>Fecha de lectura de la tesis:<\/strong>\u00a0 01\/01\/1996<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<h3>Direcci\u00f3n y tribunal<\/h3>\n<ul>\n<li><strong>Director de la tesis<\/strong>\n<ul>\n<li>Carlos Dieguez Gonzalez<\/li>\n<\/ul>\n<\/li>\n<li><strong>Tribunal<\/strong>\n<ul>\n<li>Presidente del tribunal: Felipe Casanueva Freijo <\/li>\n<li>M\u00aa Josefa Toro Nozal (vocal)<\/li>\n<li>Fernando Dominguez Puente (vocal)<\/li>\n<li>Angela Pe\u00f1alva Maqueda (vocal)<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Tesis doctoral de Raquel Coya Guerrero El objetivo de este trabajo ha sido estudiar el papel regulador del tgf-beta1 sobre [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"site-sidebar-layout":"default","site-content-layout":"","ast-site-content-layout":"","site-content-style":"default","site-sidebar-style":"default","ast-global-header-display":"","ast-banner-title-visibility":"","ast-main-header-display":"","ast-hfb-above-header-display":"","ast-hfb-below-header-display":"","ast-hfb-mobile-header-display":"","site-post-title":"","ast-breadcrumbs-content":"","ast-featured-img":"","footer-sml-layout":"","theme-transparent-header-meta":"","adv-header-id-meta":"","stick-header-meta":"","header-above-stick-meta":"","header-main-stick-meta":"","header-below-stick-meta":"","astra-migrate-meta-layouts":"default","ast-page-background-enabled":"default","ast-page-background-meta":{"desktop":{"background-color":"var(--ast-global-color-4)","background-image":"","background-repeat":"repeat","background-position":"center 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