Q3142666 (Q3142666): Difference between revisions
Jump to navigation
Jump to search
(Changed an Item: Edited by the materialized bot - inferring region from the coordinates) |
(Created claim: summary (P836): IN ANAPHASE THE TWO COPIES OF THE REPLICATED CHROMOSOMES ARE SEPARATED AND SEGREGATED TO THE DAUGHTER CELLS. CERTAIN GENETIC MUTATIONS THAT AFFECT CODING GENES FOR TOPOISOMERASE II, CONDENSINE COMPLEX, SMC5/6, SEPARASA, BLOOM SYNDROME PROTEIN, FANCONI ANEMIA COMPLEX PROTEINS, STRUCTURE-SPECIFIC ENDONUCLEASES OR CELL CYCLE CONTROL POINT PROTEINS (CHECKPOINTS) CAUSE CHROMOSOMAL BRIDGES IN ANAPHASE. ALSO CERTAIN CHROMOSOMAL REARRANGEMENTS SUCH AS D...) |
||||||||||||||
| Property / summary | |||||||||||||||
IN ANAPHASE THE TWO COPIES OF THE REPLICATED CHROMOSOMES ARE SEPARATED AND SEGREGATED TO THE DAUGHTER CELLS. CERTAIN GENETIC MUTATIONS THAT AFFECT CODING GENES FOR TOPOISOMERASE II, CONDENSINE COMPLEX, SMC5/6, SEPARASA, BLOOM SYNDROME PROTEIN, FANCONI ANEMIA COMPLEX PROTEINS, STRUCTURE-SPECIFIC ENDONUCLEASES OR CELL CYCLE CONTROL POINT PROTEINS (CHECKPOINTS) CAUSE CHROMOSOMAL BRIDGES IN ANAPHASE. ALSO CERTAIN CHROMOSOMAL REARRANGEMENTS SUCH AS DICENTRIC CHROMOSOMES, CHEMICAL AGENTS (E.G. TOPOISOMERASE OR CHECKPOINT INHIBITORS), NUTRITIONAL DEFICIENCIES (FOLIC ACID) AND BIOLOGICAL TOXINS (COLIBACTIN) RESULT IN THE APPEARANCE OF ANAPHASE BRIDGES. CANCER CELLS OFTEN PRESENT THIS PHENOTYPE, TO THE EXTENT THAT THEY ARE CONSIDERED AN IMPORTANT SOURCE OF INTRATUMORAL GENETIC INSTABILITY. FOUR CAN BE THE IMMEDIATE CONSEQUENCES FOR PROGENY: (I) CYTOCINESIS ABORT (LED TO POLICENTROSOMIC tetraploids), (II) RUPTURE of DNA moleculate by cytokinesis (provoking chromosomal FUSIONS in the supervividing CELULAS), (III) UNION ROTURE TO THE FAZ OF MICROTUBULS (leaving MONOSOMIA and trisomyas) AND (IV) DEATH in this memory we present a project to be held in the state of the anaphylactic consents of the offspring for the offspring, as soon as possible (in the child-resulting CELULAS of anomaly) as long as possible. PLAZO (PATRON OF GENETIC REOORDENAMENTS OF THE SUPERVIVENT progeny) IN THE ORGANISM SACCHAROMYCES CEREVISIAE MODEL. WE ALSO PROPOSE TO ASSESS THE POSSIBLE BENEFICIAL EFFECT OF CHEMICALLY INDUCING MORE ANAPHASE BRIDGES IN THOSE CELLS WHERE THERE ARE ALREADY UNDERLYING GENETIC DEFECTS THAT FAVOR THEM. THAT IS, TO ASSESS THE MITOTIC CATASTROPHE ASSOCIATED WITH ANAPHASE BRIDGES AS AN ANTITUMOR STRATEGY. IT IS A CONTINUATION AND EXPANSION OF OUR PREVIOUS STUDIES ON THE GENETIC CAUSES OF THESE BRIDGES AND THEIR PHYSICAL AND SCIENTIFIC CHARACTERISATION, AS WELL AS THE SEARCH FOR CHEMICAL AGENTS THAT FAVOR THEIR APPEARANCE (ESSENTIALLY CATALITIC INHIBITORS OF TOPOISOMERASE II). _x000D_ the PLANT MEMORY OF THE THIRD GENERAL OBJECTIVES:_x000D_ 1) Determining the consequences for the progeny of several models of anaphase poles that differ in (I) the quantity of affixed chromosomes, (II) The PURURALITY OF UNIONS, (III) Ploidia DE LA CELULAS, (IV) COINCIDENT PRESENCE OF GENOTOXIC DAY (e.g. AGENTS ALQUILANTES), (V) PRESENCE OF DEFECTS IN THE REPARATION OF DAMY to DNA, AND (VI) PRESENCE OF DEFECTS IN ANAFASE checkpoints (NoCut, mid-ANAPHASE AND SPINDLE POSITION?_x000D_ 2) BETWEEN THE CAUSES AND CONSEQUENCES OF ANAFASE POINTS FOR INTERMEDIARY OF DAMY REPARATION to DNA. IN PARTICULAR BRIDGES DUE TO DEFICIENCY IN BLOOM SYNDROME PROTEIN HOMOLOGES, FANCONI ANEMIA GROUP M, AND OTHER NON-ESSENTIAL HELICASES. _x000D_ 3) PROFUNDING IN THE CHARACTERISATION OF NEW CATALITICAL INHIBITORS OF TOPOisomerase II AND IDENTIFICATIONS (and in those new ones who are swept from branded COLABORATIONS). EVALUATE OTHER POSSIBLE BIOLOGICAL ACTIVITIES OF THESE SUBSTANCES, AND THEIR CYTOTOXIC AND PLEIOTROPIC EFFECTS IN EUKARYOTIC AND PROKARYOTIC CELL MODELS. (English) | |||||||||||||||
| Property / summary: IN ANAPHASE THE TWO COPIES OF THE REPLICATED CHROMOSOMES ARE SEPARATED AND SEGREGATED TO THE DAUGHTER CELLS. CERTAIN GENETIC MUTATIONS THAT AFFECT CODING GENES FOR TOPOISOMERASE II, CONDENSINE COMPLEX, SMC5/6, SEPARASA, BLOOM SYNDROME PROTEIN, FANCONI ANEMIA COMPLEX PROTEINS, STRUCTURE-SPECIFIC ENDONUCLEASES OR CELL CYCLE CONTROL POINT PROTEINS (CHECKPOINTS) CAUSE CHROMOSOMAL BRIDGES IN ANAPHASE. ALSO CERTAIN CHROMOSOMAL REARRANGEMENTS SUCH AS DICENTRIC CHROMOSOMES, CHEMICAL AGENTS (E.G. TOPOISOMERASE OR CHECKPOINT INHIBITORS), NUTRITIONAL DEFICIENCIES (FOLIC ACID) AND BIOLOGICAL TOXINS (COLIBACTIN) RESULT IN THE APPEARANCE OF ANAPHASE BRIDGES. CANCER CELLS OFTEN PRESENT THIS PHENOTYPE, TO THE EXTENT THAT THEY ARE CONSIDERED AN IMPORTANT SOURCE OF INTRATUMORAL GENETIC INSTABILITY. FOUR CAN BE THE IMMEDIATE CONSEQUENCES FOR PROGENY: (I) CYTOCINESIS ABORT (LED TO POLICENTROSOMIC tetraploids), (II) RUPTURE of DNA moleculate by cytokinesis (provoking chromosomal FUSIONS in the supervividing CELULAS), (III) UNION ROTURE TO THE FAZ OF MICROTUBULS (leaving MONOSOMIA and trisomyas) AND (IV) DEATH in this memory we present a project to be held in the state of the anaphylactic consents of the offspring for the offspring, as soon as possible (in the child-resulting CELULAS of anomaly) as long as possible. PLAZO (PATRON OF GENETIC REOORDENAMENTS OF THE SUPERVIVENT progeny) IN THE ORGANISM SACCHAROMYCES CEREVISIAE MODEL. WE ALSO PROPOSE TO ASSESS THE POSSIBLE BENEFICIAL EFFECT OF CHEMICALLY INDUCING MORE ANAPHASE BRIDGES IN THOSE CELLS WHERE THERE ARE ALREADY UNDERLYING GENETIC DEFECTS THAT FAVOR THEM. THAT IS, TO ASSESS THE MITOTIC CATASTROPHE ASSOCIATED WITH ANAPHASE BRIDGES AS AN ANTITUMOR STRATEGY. IT IS A CONTINUATION AND EXPANSION OF OUR PREVIOUS STUDIES ON THE GENETIC CAUSES OF THESE BRIDGES AND THEIR PHYSICAL AND SCIENTIFIC CHARACTERISATION, AS WELL AS THE SEARCH FOR CHEMICAL AGENTS THAT FAVOR THEIR APPEARANCE (ESSENTIALLY CATALITIC INHIBITORS OF TOPOISOMERASE II). _x000D_ the PLANT MEMORY OF THE THIRD GENERAL OBJECTIVES:_x000D_ 1) Determining the consequences for the progeny of several models of anaphase poles that differ in (I) the quantity of affixed chromosomes, (II) The PURURALITY OF UNIONS, (III) Ploidia DE LA CELULAS, (IV) COINCIDENT PRESENCE OF GENOTOXIC DAY (e.g. AGENTS ALQUILANTES), (V) PRESENCE OF DEFECTS IN THE REPARATION OF DAMY to DNA, AND (VI) PRESENCE OF DEFECTS IN ANAFASE checkpoints (NoCut, mid-ANAPHASE AND SPINDLE POSITION?_x000D_ 2) BETWEEN THE CAUSES AND CONSEQUENCES OF ANAFASE POINTS FOR INTERMEDIARY OF DAMY REPARATION to DNA. IN PARTICULAR BRIDGES DUE TO DEFICIENCY IN BLOOM SYNDROME PROTEIN HOMOLOGES, FANCONI ANEMIA GROUP M, AND OTHER NON-ESSENTIAL HELICASES. _x000D_ 3) PROFUNDING IN THE CHARACTERISATION OF NEW CATALITICAL INHIBITORS OF TOPOisomerase II AND IDENTIFICATIONS (and in those new ones who are swept from branded COLABORATIONS). EVALUATE OTHER POSSIBLE BIOLOGICAL ACTIVITIES OF THESE SUBSTANCES, AND THEIR CYTOTOXIC AND PLEIOTROPIC EFFECTS IN EUKARYOTIC AND PROKARYOTIC CELL MODELS. (English) / rank | |||||||||||||||
Normal rank | |||||||||||||||
| Property / summary: IN ANAPHASE THE TWO COPIES OF THE REPLICATED CHROMOSOMES ARE SEPARATED AND SEGREGATED TO THE DAUGHTER CELLS. CERTAIN GENETIC MUTATIONS THAT AFFECT CODING GENES FOR TOPOISOMERASE II, CONDENSINE COMPLEX, SMC5/6, SEPARASA, BLOOM SYNDROME PROTEIN, FANCONI ANEMIA COMPLEX PROTEINS, STRUCTURE-SPECIFIC ENDONUCLEASES OR CELL CYCLE CONTROL POINT PROTEINS (CHECKPOINTS) CAUSE CHROMOSOMAL BRIDGES IN ANAPHASE. ALSO CERTAIN CHROMOSOMAL REARRANGEMENTS SUCH AS DICENTRIC CHROMOSOMES, CHEMICAL AGENTS (E.G. TOPOISOMERASE OR CHECKPOINT INHIBITORS), NUTRITIONAL DEFICIENCIES (FOLIC ACID) AND BIOLOGICAL TOXINS (COLIBACTIN) RESULT IN THE APPEARANCE OF ANAPHASE BRIDGES. CANCER CELLS OFTEN PRESENT THIS PHENOTYPE, TO THE EXTENT THAT THEY ARE CONSIDERED AN IMPORTANT SOURCE OF INTRATUMORAL GENETIC INSTABILITY. FOUR CAN BE THE IMMEDIATE CONSEQUENCES FOR PROGENY: (I) CYTOCINESIS ABORT (LED TO POLICENTROSOMIC tetraploids), (II) RUPTURE of DNA moleculate by cytokinesis (provoking chromosomal FUSIONS in the supervividing CELULAS), (III) UNION ROTURE TO THE FAZ OF MICROTUBULS (leaving MONOSOMIA and trisomyas) AND (IV) DEATH in this memory we present a project to be held in the state of the anaphylactic consents of the offspring for the offspring, as soon as possible (in the child-resulting CELULAS of anomaly) as long as possible. PLAZO (PATRON OF GENETIC REOORDENAMENTS OF THE SUPERVIVENT progeny) IN THE ORGANISM SACCHAROMYCES CEREVISIAE MODEL. WE ALSO PROPOSE TO ASSESS THE POSSIBLE BENEFICIAL EFFECT OF CHEMICALLY INDUCING MORE ANAPHASE BRIDGES IN THOSE CELLS WHERE THERE ARE ALREADY UNDERLYING GENETIC DEFECTS THAT FAVOR THEM. THAT IS, TO ASSESS THE MITOTIC CATASTROPHE ASSOCIATED WITH ANAPHASE BRIDGES AS AN ANTITUMOR STRATEGY. IT IS A CONTINUATION AND EXPANSION OF OUR PREVIOUS STUDIES ON THE GENETIC CAUSES OF THESE BRIDGES AND THEIR PHYSICAL AND SCIENTIFIC CHARACTERISATION, AS WELL AS THE SEARCH FOR CHEMICAL AGENTS THAT FAVOR THEIR APPEARANCE (ESSENTIALLY CATALITIC INHIBITORS OF TOPOISOMERASE II). _x000D_ the PLANT MEMORY OF THE THIRD GENERAL OBJECTIVES:_x000D_ 1) Determining the consequences for the progeny of several models of anaphase poles that differ in (I) the quantity of affixed chromosomes, (II) The PURURALITY OF UNIONS, (III) Ploidia DE LA CELULAS, (IV) COINCIDENT PRESENCE OF GENOTOXIC DAY (e.g. AGENTS ALQUILANTES), (V) PRESENCE OF DEFECTS IN THE REPARATION OF DAMY to DNA, AND (VI) PRESENCE OF DEFECTS IN ANAFASE checkpoints (NoCut, mid-ANAPHASE AND SPINDLE POSITION?_x000D_ 2) BETWEEN THE CAUSES AND CONSEQUENCES OF ANAFASE POINTS FOR INTERMEDIARY OF DAMY REPARATION to DNA. IN PARTICULAR BRIDGES DUE TO DEFICIENCY IN BLOOM SYNDROME PROTEIN HOMOLOGES, FANCONI ANEMIA GROUP M, AND OTHER NON-ESSENTIAL HELICASES. _x000D_ 3) PROFUNDING IN THE CHARACTERISATION OF NEW CATALITICAL INHIBITORS OF TOPOisomerase II AND IDENTIFICATIONS (and in those new ones who are swept from branded COLABORATIONS). EVALUATE OTHER POSSIBLE BIOLOGICAL ACTIVITIES OF THESE SUBSTANCES, AND THEIR CYTOTOXIC AND PLEIOTROPIC EFFECTS IN EUKARYOTIC AND PROKARYOTIC CELL MODELS. (English) / qualifier | |||||||||||||||
point in time: 12 October 2021
| |||||||||||||||
Revision as of 13:58, 12 October 2021
Project Q3142666 in Spain
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | No label defined |
Project Q3142666 in Spain |
Statements
82,280.0 Euro
0 references
96,800.0 Euro
0 references
85.0 percent
0 references
1 January 2016
0 references
31 December 2018
0 references
FUNDACION CANARIA DE INVESTIGACION SANITARIA (FUNCANIS)
0 references
28°28'10.74"N, 16°15'14.72"W
0 references
38038
0 references
EN ANAFASE LAS DOS COPIAS DE LOS CROMOSOMAS REPLICADOS SON SEPARADAS Y SEGREGADAS A LAS CELULAS HIJAS. CIERTAS MUTACIONES GENETICAS QUE AFECTAN A LOS GENES CODIFICANTES PARA LA TOPOISOMERASA II, EL COMPLEJO CONDENSINA, EL COMPLEJO SMC5/6, LA SEPARASA, LA PROTEINA DEL SINDROME DE BLOOM, PROTEINAS DEL COMPLEJO DE LA ANEMIA DE FANCONI, ENDONUCLEASAS ESPECIFICAS DE ESTRUCTURA O PROTEINAS DE PUNTOS DE CONTROL DEL CICLO CELULAR (¿CHECKPOINTS¿) OCASIONAN PUENTES CROMOSOMICOS EN ANAFASE. TAMBIEN CIERTOS REORDENAMIENTOS CROMOSOMICOS COMO LOS CROMOSOMAS DICENTRICOS, AGENTES QUIMICOS (P. EJ. INHIBIDORES DE LAS TOPOISOMERASAS O DE LOS CHECKPOINTS), DEFICIENCIAS NUTRICIONALES (ACIDO FOLICO) Y TOXINAS BIOLOGICAS (COLIBACTINA) DAN LUGAR A LA APARICION DE PUENTES DE ANAFASE. LAS CELULAS CANCERIGENAS PRESENTAN FRECUENTEMENTE ESTE FENOTIPO, HASTA EL PUNTO QUE SE LOS CONSIDERA UNA FUENTE IMPORTANTE DE INESTABILIDAD GENETICA INTRATUMORAL. CUATRO PUEDEN SER LAS CONSECUENCIAS INMEDIATAS PARA LA PROGENIE: (I) ABORTO DE LA CITOCINESIS (DA LUGAR A TETRAPLOIDES POLICENTROSOMICOS), (II) RUPTURA DE LA MOLECULA DE ADN POR LA CITOCINESIS (PROVOCARA FUSIONES CROMOSOMICAS EN LAS CELULAS SUPERVIVIENTES), (III) ROTURA DE LA UNION AL HAZ DE MICROTUBULOS (DA LUGAR A MONOSOMIAS Y TRISOMIAS) Y (IV) MUERTE DE LA CELULA HIJA (YA SEA DE FORMA ACCIDENTAL O PROGRAMADA)._x000D_ EN ESTA MEMORIA PRESENTAMOS UN PROYECTO QUE SE CENTRA EN EL ESTUDIO DE LAS CONSECUENCIAS DE LOS PUENTES DE ANAFASE PARA LA PROGENIE, TANTO INMEDIATA (EN LAS CELULAS HIJAS RESULTANTES DE LA ANAFASE ANOMALA) COMO A LARGO PLAZO (PATRON DE REOORDENAMIENTOS GENETICOS DE LA PROGENIE SUPERVIVIENTE) EN LA ORGANISMO MODELO SACCHAROMYCES CEREVISIAE. TAMBIEN PLANTEAMOS VALORAR EL POSIBLE EFECTO BENEFICIOSO DE INDUCIR QUIMICAMENTE MAS PUENTES DE ANAFASE EN AQUELLAS CELULAS DONDE YA EXISTAN DEFECTOS GENETICOS SUBYACENTES QUE LOS FAVORECEN. ESTO ES, VALORAR LA CATASTROFE MITOTICA ASOCIADA A PUENTES DE ANAFASE COMO ESTRATEGIA ANTITUMORAL. ES UNA CONTINUACION Y AMPLIACION DE NUESTROS ESTUDIOS PREVIOS SOBRE LAS CAUSAS GENETICAS DE ESTOS PUENTES Y SU CARACTERIZACION FISICA Y CITOLOGICA, ASI COMO LA BUSQUEDA DE AGENTES QUIMICOS QUE FAVOREZCAN SU APARICION (FUNDAMENTALMENTE INHIBIDORES CATALITICOS DE LA TOPOISOMERASA II). _x000D_ LA MEMORIA PLANTEA LOS TRES SIGUIENTES OBJETIVOS GENERALES:_x000D_ 1) DETERMINAR LAS CONSECUENCIAS PARA LA PROGENIE DE VARIOS MODELOS DE PUENTES DE ANAFASE QUE SE DIFERENCIAN EN (I) LA CANTIDAD DE CROMOSOMAS AFECTADOS, (II) LA NATURALEZA FISICA DE LAS UNIONES, (III) PLOIDIA DE LAS CELULAS, (IV) PRESENCIA COINCIDENTE DE DAÑO GENOTOXICO (P. EJ. AGENTES ALQUILANTES), (V) PRESENCIA DE DEFECTOS EN LA REPARACION DEL DAÑO AL ADN, Y (VI) PRESENCIA DE DEFECTOS EN LOS CHECKPOINTS DE ANAFASE (¿NOCUT¿, ¿MID-ANAPHASE¿ Y ¿SPINDLE POSITION¿)._x000D_ 2) ENTENDER MEJOR LAS CAUSAS Y CONSECUENCIAS DE LOS PUENTES DE ANAFASE FORMADOS POR INTERMEDIARIOS DE LA REPARACION DEL DAÑO AL ADN. EN ESPECIAL LOS PUENTES DEBIDOS A LA DEFICIENCIA EN LOS HOMOLOGOS A LA PROTEINA DEL SINDROME DE BLOOM, DEL GRUPO M DE LA ANEMIA DE FANCONI, Y DE OTRAS HELICASAS NO ESENCIALES. _x000D_ 3) PROFUNDIZAR EN LA CARACTERIZACION DE LOS NUEVOS INHIBIDORES CATALITICOS DE LA TOPOISOMERASA II YA IDENTIFICADOS (Y EN AQUELLOS NUEVOS QUE SURJAN DE LAS COLABORACIONES EN MARCHA). EVALUAR OTRAS POSIBLES ACTIVIDADES BIOLOGICAS DE DICHAS SUSTANCIAS, Y SUS EFECTOS CITOTOXICOS Y PLEIOTROPICOS EN MODELOS CELULARES EUCARIOTAS Y PROCARIOTAS. (Spanish)
0 references
IN ANAPHASE THE TWO COPIES OF THE REPLICATED CHROMOSOMES ARE SEPARATED AND SEGREGATED TO THE DAUGHTER CELLS. CERTAIN GENETIC MUTATIONS THAT AFFECT CODING GENES FOR TOPOISOMERASE II, CONDENSINE COMPLEX, SMC5/6, SEPARASA, BLOOM SYNDROME PROTEIN, FANCONI ANEMIA COMPLEX PROTEINS, STRUCTURE-SPECIFIC ENDONUCLEASES OR CELL CYCLE CONTROL POINT PROTEINS (CHECKPOINTS) CAUSE CHROMOSOMAL BRIDGES IN ANAPHASE. ALSO CERTAIN CHROMOSOMAL REARRANGEMENTS SUCH AS DICENTRIC CHROMOSOMES, CHEMICAL AGENTS (E.G. TOPOISOMERASE OR CHECKPOINT INHIBITORS), NUTRITIONAL DEFICIENCIES (FOLIC ACID) AND BIOLOGICAL TOXINS (COLIBACTIN) RESULT IN THE APPEARANCE OF ANAPHASE BRIDGES. CANCER CELLS OFTEN PRESENT THIS PHENOTYPE, TO THE EXTENT THAT THEY ARE CONSIDERED AN IMPORTANT SOURCE OF INTRATUMORAL GENETIC INSTABILITY. FOUR CAN BE THE IMMEDIATE CONSEQUENCES FOR PROGENY: (I) CYTOCINESIS ABORT (LED TO POLICENTROSOMIC tetraploids), (II) RUPTURE of DNA moleculate by cytokinesis (provoking chromosomal FUSIONS in the supervividing CELULAS), (III) UNION ROTURE TO THE FAZ OF MICROTUBULS (leaving MONOSOMIA and trisomyas) AND (IV) DEATH in this memory we present a project to be held in the state of the anaphylactic consents of the offspring for the offspring, as soon as possible (in the child-resulting CELULAS of anomaly) as long as possible. PLAZO (PATRON OF GENETIC REOORDENAMENTS OF THE SUPERVIVENT progeny) IN THE ORGANISM SACCHAROMYCES CEREVISIAE MODEL. WE ALSO PROPOSE TO ASSESS THE POSSIBLE BENEFICIAL EFFECT OF CHEMICALLY INDUCING MORE ANAPHASE BRIDGES IN THOSE CELLS WHERE THERE ARE ALREADY UNDERLYING GENETIC DEFECTS THAT FAVOR THEM. THAT IS, TO ASSESS THE MITOTIC CATASTROPHE ASSOCIATED WITH ANAPHASE BRIDGES AS AN ANTITUMOR STRATEGY. IT IS A CONTINUATION AND EXPANSION OF OUR PREVIOUS STUDIES ON THE GENETIC CAUSES OF THESE BRIDGES AND THEIR PHYSICAL AND SCIENTIFIC CHARACTERISATION, AS WELL AS THE SEARCH FOR CHEMICAL AGENTS THAT FAVOR THEIR APPEARANCE (ESSENTIALLY CATALITIC INHIBITORS OF TOPOISOMERASE II). _x000D_ the PLANT MEMORY OF THE THIRD GENERAL OBJECTIVES:_x000D_ 1) Determining the consequences for the progeny of several models of anaphase poles that differ in (I) the quantity of affixed chromosomes, (II) The PURURALITY OF UNIONS, (III) Ploidia DE LA CELULAS, (IV) COINCIDENT PRESENCE OF GENOTOXIC DAY (e.g. AGENTS ALQUILANTES), (V) PRESENCE OF DEFECTS IN THE REPARATION OF DAMY to DNA, AND (VI) PRESENCE OF DEFECTS IN ANAFASE checkpoints (NoCut, mid-ANAPHASE AND SPINDLE POSITION?_x000D_ 2) BETWEEN THE CAUSES AND CONSEQUENCES OF ANAFASE POINTS FOR INTERMEDIARY OF DAMY REPARATION to DNA. IN PARTICULAR BRIDGES DUE TO DEFICIENCY IN BLOOM SYNDROME PROTEIN HOMOLOGES, FANCONI ANEMIA GROUP M, AND OTHER NON-ESSENTIAL HELICASES. _x000D_ 3) PROFUNDING IN THE CHARACTERISATION OF NEW CATALITICAL INHIBITORS OF TOPOisomerase II AND IDENTIFICATIONS (and in those new ones who are swept from branded COLABORATIONS). EVALUATE OTHER POSSIBLE BIOLOGICAL ACTIVITIES OF THESE SUBSTANCES, AND THEIR CYTOTOXIC AND PLEIOTROPIC EFFECTS IN EUKARYOTIC AND PROKARYOTIC CELL MODELS. (English)
12 October 2021
0 references
Santa Cruz de Tenerife
0 references
Identifiers
BFU2015-63902-R
0 references