Q3142285 (Q3142285): Difference between revisions
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(Created claim: summary (P836): IN THIS PROJECT WE INTEND TO STUDY THE ROLE OF GCKIII KINASES (MST3, MST4 AND SOK1) AND THEIR ASSOCIATED PROTEIN, PDCD10/CCM3 IN TWO PATHOLOGICAL PROCESSES, TYPE 2 DIABETES MELLITUS AND BRAIN CAVERNOMAS. _x000D_ our PRELIMINARY RESULTS INDICATE THAT MST3 HAVE METALBOLIC EFFECTS, TANTO IN VITRO IN HEPATIC CELLS, AS IN LIVE. ITS LACK SIGNIFICANTLY DECREASES THE EXPRESSION OF GENES INVOLVED IN GLUCONEOGENESIS-PEPCK AND G6PASA- IN CULTURED CELLS, AN...) |
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IN THIS PROJECT WE INTEND TO STUDY THE ROLE OF GCKIII KINASES (MST3, MST4 AND SOK1) AND THEIR ASSOCIATED PROTEIN, PDCD10/CCM3 IN TWO PATHOLOGICAL PROCESSES, TYPE 2 DIABETES MELLITUS AND BRAIN CAVERNOMAS. _x000D_ our PRELIMINARY RESULTS INDICATE THAT MST3 HAVE METALBOLIC EFFECTS, TANTO IN VITRO IN HEPATIC CELLS, AS IN LIVE. ITS LACK SIGNIFICANTLY DECREASES THE EXPRESSION OF GENES INVOLVED IN GLUCONEOGENESIS-PEPCK AND G6PASA- IN CULTURED CELLS, AND CAUSES MICE UNDERGOING A HIGH-FAT DIET TO DECREASE GLYCEMIA AFTER FASTING AND A DECREASE IN GLUCONEOGENESIS AFTER PYRUVATE ADMINISTRATION. THIS OPENS UP THE POSSIBILITY THAT ITS MANIPULATION CAN BE USED TO CONTROL BLOOD GLUCOSE IN PATIENTS WITH TYPE 2 DIABETES, AND THAT IS WHY WE INTEND TO STUDY THE MECHANISMS BY WHICH MST3 EXERTS ITS ACTION ON GLUCONEOGENESIS, AND DEEPEN ITS IMPORTANCE IN IN VIVO MODELS. In addition, we will check whether MST3‘s METABOLICAL FUNCTIONS overlap with those of SOK1, for which METABOLICAL FUNCTIONS have also been made._x000D_ YOUR PARTY, THE PROTEIN ADAPTOR CCM3 is one of the three GENES (the other CCM1 and CCM2) WHY INACTIVETION predisposes the development of these CEREBRAL cavernous malformations, and when I’m going to help us understand the pathogy and pathology of these disasters. THEIR ABSENCE PREDISPOSES THE DEVELOPMENT OF CAVERNOUS MALFORMATIONS THROUGH ALTERATIONS OF ENDOTHELIAL BIOLOGY RELATED TO GCKIII KINASES. THESE ALTERATIONS MAY BE CELLULAR ADHESION, AS CCM3 HAS BEEN FOUND IN FOCAL ADHESIONS; MEMBRANE TRAFFICKING AND AUTOPHAGIA, PROCESSES IN WHICH WE KNOW THAT CCM3 IS INVOLVED; AND/OR THE ABNORMAL RESPONSE TO MECHANICAL STIMULI OF CELLS, BOTH WHEN THEY FORM A STATIC MONOLAYER AND WHEN THEY UNDERGO FLOW, RESPONSES THAT APPEAR ABNORMAL ACCORDING TO OUR PRELIMINARY RESULTS. We intend to study as the GCKIII, CCM3 (and the other GENES that support the development of cavernomas, CCM1 and CCM2), AFECTING THE CELLAR ADHESION, AUTOFAGIA, THE TRAFFIC OF MEMBRANAS AND THE RESPONSE to MECHANICAL STIMULES, and as this is related to the development of cavernomes and the endothelial-mesenchyma translation that is known to be covered by these lesions._x000D_ IN DEFINITIVE, IN THE PROJECT we will apply the EXPERIENCE that our research group has been accumulating in the last years in BASICA CELL BASIC BIOLOGY to the state of two very important pathological products, providing an ALTERNATIVE approximation to other STUDIES, which can carry new and important aspectos to our knowledge of the same and potential new approaches. (English) | |||||||||||||||
| Property / summary: IN THIS PROJECT WE INTEND TO STUDY THE ROLE OF GCKIII KINASES (MST3, MST4 AND SOK1) AND THEIR ASSOCIATED PROTEIN, PDCD10/CCM3 IN TWO PATHOLOGICAL PROCESSES, TYPE 2 DIABETES MELLITUS AND BRAIN CAVERNOMAS. _x000D_ our PRELIMINARY RESULTS INDICATE THAT MST3 HAVE METALBOLIC EFFECTS, TANTO IN VITRO IN HEPATIC CELLS, AS IN LIVE. ITS LACK SIGNIFICANTLY DECREASES THE EXPRESSION OF GENES INVOLVED IN GLUCONEOGENESIS-PEPCK AND G6PASA- IN CULTURED CELLS, AND CAUSES MICE UNDERGOING A HIGH-FAT DIET TO DECREASE GLYCEMIA AFTER FASTING AND A DECREASE IN GLUCONEOGENESIS AFTER PYRUVATE ADMINISTRATION. THIS OPENS UP THE POSSIBILITY THAT ITS MANIPULATION CAN BE USED TO CONTROL BLOOD GLUCOSE IN PATIENTS WITH TYPE 2 DIABETES, AND THAT IS WHY WE INTEND TO STUDY THE MECHANISMS BY WHICH MST3 EXERTS ITS ACTION ON GLUCONEOGENESIS, AND DEEPEN ITS IMPORTANCE IN IN VIVO MODELS. In addition, we will check whether MST3‘s METABOLICAL FUNCTIONS overlap with those of SOK1, for which METABOLICAL FUNCTIONS have also been made._x000D_ YOUR PARTY, THE PROTEIN ADAPTOR CCM3 is one of the three GENES (the other CCM1 and CCM2) WHY INACTIVETION predisposes the development of these CEREBRAL cavernous malformations, and when I’m going to help us understand the pathogy and pathology of these disasters. THEIR ABSENCE PREDISPOSES THE DEVELOPMENT OF CAVERNOUS MALFORMATIONS THROUGH ALTERATIONS OF ENDOTHELIAL BIOLOGY RELATED TO GCKIII KINASES. THESE ALTERATIONS MAY BE CELLULAR ADHESION, AS CCM3 HAS BEEN FOUND IN FOCAL ADHESIONS; MEMBRANE TRAFFICKING AND AUTOPHAGIA, PROCESSES IN WHICH WE KNOW THAT CCM3 IS INVOLVED; AND/OR THE ABNORMAL RESPONSE TO MECHANICAL STIMULI OF CELLS, BOTH WHEN THEY FORM A STATIC MONOLAYER AND WHEN THEY UNDERGO FLOW, RESPONSES THAT APPEAR ABNORMAL ACCORDING TO OUR PRELIMINARY RESULTS. We intend to study as the GCKIII, CCM3 (and the other GENES that support the development of cavernomas, CCM1 and CCM2), AFECTING THE CELLAR ADHESION, AUTOFAGIA, THE TRAFFIC OF MEMBRANAS AND THE RESPONSE to MECHANICAL STIMULES, and as this is related to the development of cavernomes and the endothelial-mesenchyma translation that is known to be covered by these lesions._x000D_ IN DEFINITIVE, IN THE PROJECT we will apply the EXPERIENCE that our research group has been accumulating in the last years in BASICA CELL BASIC BIOLOGY to the state of two very important pathological products, providing an ALTERNATIVE approximation to other STUDIES, which can carry new and important aspectos to our knowledge of the same and potential new approaches. (English) / rank | |||||||||||||||
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| Property / summary: IN THIS PROJECT WE INTEND TO STUDY THE ROLE OF GCKIII KINASES (MST3, MST4 AND SOK1) AND THEIR ASSOCIATED PROTEIN, PDCD10/CCM3 IN TWO PATHOLOGICAL PROCESSES, TYPE 2 DIABETES MELLITUS AND BRAIN CAVERNOMAS. _x000D_ our PRELIMINARY RESULTS INDICATE THAT MST3 HAVE METALBOLIC EFFECTS, TANTO IN VITRO IN HEPATIC CELLS, AS IN LIVE. ITS LACK SIGNIFICANTLY DECREASES THE EXPRESSION OF GENES INVOLVED IN GLUCONEOGENESIS-PEPCK AND G6PASA- IN CULTURED CELLS, AND CAUSES MICE UNDERGOING A HIGH-FAT DIET TO DECREASE GLYCEMIA AFTER FASTING AND A DECREASE IN GLUCONEOGENESIS AFTER PYRUVATE ADMINISTRATION. THIS OPENS UP THE POSSIBILITY THAT ITS MANIPULATION CAN BE USED TO CONTROL BLOOD GLUCOSE IN PATIENTS WITH TYPE 2 DIABETES, AND THAT IS WHY WE INTEND TO STUDY THE MECHANISMS BY WHICH MST3 EXERTS ITS ACTION ON GLUCONEOGENESIS, AND DEEPEN ITS IMPORTANCE IN IN VIVO MODELS. In addition, we will check whether MST3‘s METABOLICAL FUNCTIONS overlap with those of SOK1, for which METABOLICAL FUNCTIONS have also been made._x000D_ YOUR PARTY, THE PROTEIN ADAPTOR CCM3 is one of the three GENES (the other CCM1 and CCM2) WHY INACTIVETION predisposes the development of these CEREBRAL cavernous malformations, and when I’m going to help us understand the pathogy and pathology of these disasters. THEIR ABSENCE PREDISPOSES THE DEVELOPMENT OF CAVERNOUS MALFORMATIONS THROUGH ALTERATIONS OF ENDOTHELIAL BIOLOGY RELATED TO GCKIII KINASES. THESE ALTERATIONS MAY BE CELLULAR ADHESION, AS CCM3 HAS BEEN FOUND IN FOCAL ADHESIONS; MEMBRANE TRAFFICKING AND AUTOPHAGIA, PROCESSES IN WHICH WE KNOW THAT CCM3 IS INVOLVED; AND/OR THE ABNORMAL RESPONSE TO MECHANICAL STIMULI OF CELLS, BOTH WHEN THEY FORM A STATIC MONOLAYER AND WHEN THEY UNDERGO FLOW, RESPONSES THAT APPEAR ABNORMAL ACCORDING TO OUR PRELIMINARY RESULTS. We intend to study as the GCKIII, CCM3 (and the other GENES that support the development of cavernomas, CCM1 and CCM2), AFECTING THE CELLAR ADHESION, AUTOFAGIA, THE TRAFFIC OF MEMBRANAS AND THE RESPONSE to MECHANICAL STIMULES, and as this is related to the development of cavernomes and the endothelial-mesenchyma translation that is known to be covered by these lesions._x000D_ IN DEFINITIVE, IN THE PROJECT we will apply the EXPERIENCE that our research group has been accumulating in the last years in BASICA CELL BASIC BIOLOGY to the state of two very important pathological products, providing an ALTERNATIVE approximation to other STUDIES, which can carry new and important aspectos to our knowledge of the same and potential new approaches. (English) / qualifier | |||||||||||||||
point in time: 12 October 2021
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Revision as of 13:38, 12 October 2021
Project Q3142285 in Spain
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | No label defined |
Project Q3142285 in Spain |
Statements
96,800.0 Euro
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121,000.0 Euro
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80.0 percent
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1 January 2015
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31 March 2018
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UNIVERSIDAD DE SANTIAGO DE COMPOSTELA
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42°52'49.51"N, 8°32'45.10"W
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15078
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EN ESTE PROYECTO NOS PROPONEMOS ESTUDIAR EL PAPEL DE LAS QUINASAS GCKIII (MST3, MST4 Y SOK1) Y SU PROTEINA ASOCIADA, PDCD10/CCM3 EN DOS PROCESOS PATOLOGICOS, LA DIABETES MELLITUS TIPO 2 Y LOS CAVERNOMAS CEREBRALES. _x000D_ NUESTROS RESULTADOS PRELIMINARES INDICAN QUE MST3 TIENE CLAROS EFECTOS METABOLICOS, TANTO IN VITRO EN CELULAS HEPATICAS, COMO IN VIVO. SU FALTA DISMINUYE SIGNIFICATIVAMENTE LA EXPRESION DE LOS GENES IMPLICADOS EN LA GLUCONEOGENESIS-PEPCK Y G6PASA- EN CELULAS EN CULTIVO, Y PROVOCA EN RATONES SOMETIDOS A UNA DIETA ALTA EN GRASA UNA DISMINUCION DE LA GLUCEMIA TRAS AYUNO Y UNA DISMINUCION DE LA GLUCONEOGENESIS TRAS LA ADMINISTRACION DE PIRUVATO. ESTO ABRE LA POSIBILIDAD DE QUE SU MANIPULACION PUEDA SERVIR PARA CONTROLAR LA GLUCEMIA EN PACIENTES CON DIABETES TIPO 2, Y POR ESO NOS PROPONEMOS ESTUDIAR LOS MECANISMOS POR LOS QUE MST3 EJERCE SU ACCION SOBRE LA GLUCONEOGENESIS, Y PROFUNDIZAR EN SU IMPORTANCIA EN MODELOS IN VIVO. ADEMAS, COMPROBAREMOS SI LAS FUNCIONES METABOLICAS DE MST3 SE SOLAPAN CON LAS DE SOK1, PARA LA QUE SE HAN DESCRITO TAMBIEN FUNCIONES METABOLICAS._x000D_ POR SU PARTE, LA PROTEINA ADAPTADORA CCM3 ES UNO DE LOS TRES GENES (LOS OTROS SON CCM1 Y CCM2) CUYA INACTIVACION PREDISPONE AL DESARROLLO DE ESTAS MALFORMACIONES CAVERNOSAS CEREBRALES, Y CUYO ESTUDIO NOS ESTA AYUDANDO A ENTENDER LA PATOGENIA Y FISIOPATOLOGIA DE ESTAS LESIONES. SU AUSENCIA PREDISPONE AL DESARROLLO DE MALFORMACIONES CAVERNOSAS A TRAVES DE ALTERACIONES DE LA BIOLOGIA ENDOTELIAL RELACIONADAS CON LAS QUINASAS GCKIII. ESTAS ALTERACIONES PUEDEN SER LA ADHESION CELULAR, YA QUE CCM3 SE HA ENCONTRADO EN LAS ADHESIONES FOCALES; EL TRAFICO DE MEMBRANAS Y AUTOFAGIA, PROCESOS EN LOS SABEMOS QUE INTERVIENE CCM3; Y/O LA RESPUESTA ANORMAL A ESTIMULOS MECANICOS DE LAS CELULAS, TANTO CUANDO FORMAN UNA MONOCAPA ESTATICA COMO CUANDO SE SOMETEN A FLUJO, RESPUESTAS QUE APARECEN ANORMALES SEGUN NUESTROS RESULTADOS PRELIMINARES. NOS PROPONEMOS ESTUDIAR COMO LAS GCKIII, CCM3 (Y LOS OTROS GENES QUE AFECTAN AL DESARROLLO DE CAVERNOMAS, CCM1 Y CCM2), AFECTAN A LA ADHESION CELULAR, LA AUTOFAGIA, EL TRAFICO DE MEMBRANAS Y LA RESPUESTA A ESTIMULOS MECANICOS, Y COMO SE RELACIONA ESTO CON EL DESARROLLO DE CAVERNOMAS Y LA TRANSICION ENDOTELIO-MESENQUIMA QUE SE SABE SUFREN ESTAS LESIONES._x000D_ EN DEFINITIVA, EN EL PROYECTO APLICAREMOS LA EXPERIENCIA QUE NUESTRO GRUPO DE INVESTIGACION HA IDO ACUMULANDO EN LOS ULTIMOS AÑOS EN BIOLOGIA CELULAR BASICA AL ESTUDIO DE DOS PROCESOS PATOLOGICOS MUY IMPORTANTES, APORTANDO UNA APROXIMACION ALTERNATIVA A OTROS ESTUDIOS, QUE PUEDE APORTAR NUEVOS E IMPORTANTES ASPECTOS A NUESTRO CONOCIMIENTO DE LOS MISMOS Y TAMBIEN POSIBLES APROXIMACIONES TERAPEUTICAS NOVEDOSAS. (Spanish)
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IN THIS PROJECT WE INTEND TO STUDY THE ROLE OF GCKIII KINASES (MST3, MST4 AND SOK1) AND THEIR ASSOCIATED PROTEIN, PDCD10/CCM3 IN TWO PATHOLOGICAL PROCESSES, TYPE 2 DIABETES MELLITUS AND BRAIN CAVERNOMAS. _x000D_ our PRELIMINARY RESULTS INDICATE THAT MST3 HAVE METALBOLIC EFFECTS, TANTO IN VITRO IN HEPATIC CELLS, AS IN LIVE. ITS LACK SIGNIFICANTLY DECREASES THE EXPRESSION OF GENES INVOLVED IN GLUCONEOGENESIS-PEPCK AND G6PASA- IN CULTURED CELLS, AND CAUSES MICE UNDERGOING A HIGH-FAT DIET TO DECREASE GLYCEMIA AFTER FASTING AND A DECREASE IN GLUCONEOGENESIS AFTER PYRUVATE ADMINISTRATION. THIS OPENS UP THE POSSIBILITY THAT ITS MANIPULATION CAN BE USED TO CONTROL BLOOD GLUCOSE IN PATIENTS WITH TYPE 2 DIABETES, AND THAT IS WHY WE INTEND TO STUDY THE MECHANISMS BY WHICH MST3 EXERTS ITS ACTION ON GLUCONEOGENESIS, AND DEEPEN ITS IMPORTANCE IN IN VIVO MODELS. In addition, we will check whether MST3‘s METABOLICAL FUNCTIONS overlap with those of SOK1, for which METABOLICAL FUNCTIONS have also been made._x000D_ YOUR PARTY, THE PROTEIN ADAPTOR CCM3 is one of the three GENES (the other CCM1 and CCM2) WHY INACTIVETION predisposes the development of these CEREBRAL cavernous malformations, and when I’m going to help us understand the pathogy and pathology of these disasters. THEIR ABSENCE PREDISPOSES THE DEVELOPMENT OF CAVERNOUS MALFORMATIONS THROUGH ALTERATIONS OF ENDOTHELIAL BIOLOGY RELATED TO GCKIII KINASES. THESE ALTERATIONS MAY BE CELLULAR ADHESION, AS CCM3 HAS BEEN FOUND IN FOCAL ADHESIONS; MEMBRANE TRAFFICKING AND AUTOPHAGIA, PROCESSES IN WHICH WE KNOW THAT CCM3 IS INVOLVED; AND/OR THE ABNORMAL RESPONSE TO MECHANICAL STIMULI OF CELLS, BOTH WHEN THEY FORM A STATIC MONOLAYER AND WHEN THEY UNDERGO FLOW, RESPONSES THAT APPEAR ABNORMAL ACCORDING TO OUR PRELIMINARY RESULTS. We intend to study as the GCKIII, CCM3 (and the other GENES that support the development of cavernomas, CCM1 and CCM2), AFECTING THE CELLAR ADHESION, AUTOFAGIA, THE TRAFFIC OF MEMBRANAS AND THE RESPONSE to MECHANICAL STIMULES, and as this is related to the development of cavernomes and the endothelial-mesenchyma translation that is known to be covered by these lesions._x000D_ IN DEFINITIVE, IN THE PROJECT we will apply the EXPERIENCE that our research group has been accumulating in the last years in BASICA CELL BASIC BIOLOGY to the state of two very important pathological products, providing an ALTERNATIVE approximation to other STUDIES, which can carry new and important aspectos to our knowledge of the same and potential new approaches. (English)
12 October 2021
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Santiago de Compostela
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Identifiers
SAF2014-56899-R
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