{"id":61453,"date":"2018-03-09T22:49:18","date_gmt":"2018-03-09T22:49:18","guid":{"rendered":"https:\/\/www.deberes.net\/tesis\/sin-categoria\/mecanismos-moleculares-involucrados-en-la-citotoxicidad-del-agente-antitumoral-beta-lapachona\/"},"modified":"2018-03-09T22:49:18","modified_gmt":"2018-03-09T22:49:18","slug":"mecanismos-moleculares-involucrados-en-la-citotoxicidad-del-agente-antitumoral-beta-lapachona","status":"publish","type":"post","link":"https:\/\/www.deberes.net\/tesis\/bioquimica-molecular\/mecanismos-moleculares-involucrados-en-la-citotoxicidad-del-agente-antitumoral-beta-lapachona\/","title":{"rendered":"Mecanismos moleculares involucrados en la citotoxicidad del agente antitumoral beta-lapachona."},"content":{"rendered":"<h2>Tesis doctoral de <strong>  Menacho M\u00e1rquez Mauricio Ariel <\/strong><\/h2>\n<p>Beta-lapachona ( -lap) es un agente antitumoral que induce apoptosis selectivamente en c\u00e9lulas tumorales. El mecanismo preciso de citotoxicidad de  -lap no es a\u00fan completamente comprendido. Aqu\u00ed reportamos que  -lap produce un retraso en la progresi\u00f3n del ciclo celular en la transici\u00f3n g1\/s, aumenta la fosforilaci\u00f3n de la quinasa de control rad53p y disminuye la supervivencia celular en la levadura de gemaci\u00f3n saccharomyces cerevisiae. Adem\u00e1s,  -lap induce la fosforilaci\u00f3n de histona h2a en la posici\u00f3n serina 129. Estas respuestas de control de ciclo son reguladas por las quinasas mec1p y tel1p. Mec1p se requiere para la fosforilaci\u00f3n de rad53p\/histona h2a y supervivencia celular tras tratamiento con  -lap en cultivos asincr\u00f3nicos, pero no para el retraso en la transici\u00f3n g1\/s. La mutaci\u00f3n  tel1 aumenta la sensibilidad a  -lap en una cepa defectiva en mec1, y compromete las respuestas de los puntos de control de ciclo. La fosforilaci\u00f3n de rad53p y el retraso en g1\/s son completamente dependientes de un complejo mre11p-rad50p-xrs2p (xmr) funcional, y mutantes en el complejo xmr son extremadamente sensibles al tratamiento con  -lap. Finalmente, xrs2 y tel1 trabajan epist\u00e1ticamente respecto a la sensibilidad a  -lap y xrs2p se fosforila en un modo dependiente de tel1p tras el tratamiento.  el tratamiento con  -lap tambi\u00e9n genera la producci\u00f3n de especies reactivas de ox\u00edgeno (ros), la cual es bloqueada eficientemente por dicumarol, un inhibidor de nadh deshidrogenasas (nadh-dh). El tratamiento con dicumarol no afecta a la viabilidad ni a las respuestas de control activadas por la droga. Identificamos un mutante, defectivo en la nadh-dh mitocondrial nde2p, que es resistente a la toxicidad de  -lap.  -Lap induce la producci\u00f3n de ros en este mutante, sin afectar la viabilidad o la progresi\u00f3n de ciclo. El mutante  nde2 presenta un retraso en la entrada en fase s del ciclo celular, e hipersensibilidad a agentes que da\u00f1an el adn. Nuestros datos indica<\/p>\n<p>&nbsp;<\/p>\n<h3>Datos acad\u00e9micos de la tesis doctoral \u00ab<strong>Mecanismos moleculares involucrados en la citotoxicidad del agente antitumoral beta-lapachona.<\/strong>\u00ab<\/h3>\n<ul>\n<li><strong>T\u00edtulo de la tesis:<\/strong>\u00a0 Mecanismos moleculares involucrados en la citotoxicidad del agente antitumoral beta-lapachona. <\/li>\n<li><strong>Autor:<\/strong>\u00a0  Menacho M\u00e1rquez Mauricio Ariel <\/li>\n<li><strong>Universidad:<\/strong>\u00a0 Polit\u00e9cnica de Valencia<\/li>\n<li><strong>Fecha de lectura de la tesis:<\/strong>\u00a0 22\/11\/2007<\/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> Murgu\u00eda Ib\u00e1\u00f1ez Jos\u00e9 Ram\u00f3n<\/li>\n<\/ul>\n<\/li>\n<li><strong>Tribunal<\/strong>\n<ul>\n<li>Presidente del tribunal: rosario Perona abellon <\/li>\n<li>susana Llanos giron (vocal)<\/li>\n<li>borja Belandia gomez (vocal)<\/li>\n<li>Juan  Carlos Igual Garc\u00eda (vocal)<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Tesis doctoral de Menacho M\u00e1rquez Mauricio Ariel Beta-lapachona ( -lap) es un agente antitumoral que induce apoptosis selectivamente en c\u00e9lulas [&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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