Okadaic Acid-Induced Apoptosis in Neuronal Cells: Evidence for an Abortive Mitotic Attempt
Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylatio...
Ausführliche Beschreibung
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Oxford, UK: Blackwell Science Ltd ; 1998 |
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2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 70(1998), 3, Seite 0 |
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volume:70 ; year:1998 ; number:3 ; pages:0 |
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DOI / URN: |
10.1046/j.1471-4159.1998.70031124.x |
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520 | |a Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylation of various proteins, such as the microtubule-associated protein tau. Okadaic acid induces programmed cell death in the human neuroblastoma cell lines TR14 and NT2-N, as evidenced by fragmentation of DNA and attenuation of this process by protein synthesis inhibitors. In differentiated TR14 cells, okadaic acid increases the fraction of cells in the S phase, induces the appearance of cyclin B1 and cyclin D1 markers of the cell cycle, and triggers a time-dependent increase in DNA fragmentation after release of a thymidine block. Fully differentiated NT2-N cells are forced to enter the mitotic cycle as shown by DNA staining. Chromatin condensation and chromosome formation are initiated, but the cells fail to complete their mitotic cycle. These data suggest that okadaic acid forces differentiated neuronal cells into the mitotic cycle. This pattern of cyclin up-regulation and cell cycle shift is compared with apoptosis induced by neurotrophic factor deprivation in differentiated rat pheochromocytoma PC12 cells. | ||
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10.1046/j.1471-4159.1998.70031124.x doi (DE-627)NLEJ243163142 DE-627 ger DE-627 rakwb Okadaic Acid-Induced Apoptosis in Neuronal Cells: Evidence for an Abortive Mitotic Attempt Oxford, UK Blackwell Science Ltd 1998 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylation of various proteins, such as the microtubule-associated protein tau. Okadaic acid induces programmed cell death in the human neuroblastoma cell lines TR14 and NT2-N, as evidenced by fragmentation of DNA and attenuation of this process by protein synthesis inhibitors. In differentiated TR14 cells, okadaic acid increases the fraction of cells in the S phase, induces the appearance of cyclin B1 and cyclin D1 markers of the cell cycle, and triggers a time-dependent increase in DNA fragmentation after release of a thymidine block. Fully differentiated NT2-N cells are forced to enter the mitotic cycle as shown by DNA staining. Chromatin condensation and chromosome formation are initiated, but the cells fail to complete their mitotic cycle. These data suggest that okadaic acid forces differentiated neuronal cells into the mitotic cycle. This pattern of cyclin up-regulation and cell cycle shift is compared with apoptosis induced by neurotrophic factor deprivation in differentiated rat pheochromocytoma PC12 cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Okadaic acid Nuydens, Rony oth De Jong, Mirjam oth Van Den Kieboom, Gerd oth Heers, Cara oth Dispersyn, Gwenda oth Cornelissen, Frans oth Nuyens, Roger oth Borgers, Marcel oth Geerts, Hugo oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 70(1998), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:70 year:1998 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1998.70031124.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 70 1998 3 0 |
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10.1046/j.1471-4159.1998.70031124.x doi (DE-627)NLEJ243163142 DE-627 ger DE-627 rakwb Okadaic Acid-Induced Apoptosis in Neuronal Cells: Evidence for an Abortive Mitotic Attempt Oxford, UK Blackwell Science Ltd 1998 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylation of various proteins, such as the microtubule-associated protein tau. Okadaic acid induces programmed cell death in the human neuroblastoma cell lines TR14 and NT2-N, as evidenced by fragmentation of DNA and attenuation of this process by protein synthesis inhibitors. In differentiated TR14 cells, okadaic acid increases the fraction of cells in the S phase, induces the appearance of cyclin B1 and cyclin D1 markers of the cell cycle, and triggers a time-dependent increase in DNA fragmentation after release of a thymidine block. Fully differentiated NT2-N cells are forced to enter the mitotic cycle as shown by DNA staining. Chromatin condensation and chromosome formation are initiated, but the cells fail to complete their mitotic cycle. These data suggest that okadaic acid forces differentiated neuronal cells into the mitotic cycle. This pattern of cyclin up-regulation and cell cycle shift is compared with apoptosis induced by neurotrophic factor deprivation in differentiated rat pheochromocytoma PC12 cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Okadaic acid Nuydens, Rony oth De Jong, Mirjam oth Van Den Kieboom, Gerd oth Heers, Cara oth Dispersyn, Gwenda oth Cornelissen, Frans oth Nuyens, Roger oth Borgers, Marcel oth Geerts, Hugo oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 70(1998), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:70 year:1998 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1998.70031124.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 70 1998 3 0 |
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10.1046/j.1471-4159.1998.70031124.x doi (DE-627)NLEJ243163142 DE-627 ger DE-627 rakwb Okadaic Acid-Induced Apoptosis in Neuronal Cells: Evidence for an Abortive Mitotic Attempt Oxford, UK Blackwell Science Ltd 1998 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylation of various proteins, such as the microtubule-associated protein tau. Okadaic acid induces programmed cell death in the human neuroblastoma cell lines TR14 and NT2-N, as evidenced by fragmentation of DNA and attenuation of this process by protein synthesis inhibitors. In differentiated TR14 cells, okadaic acid increases the fraction of cells in the S phase, induces the appearance of cyclin B1 and cyclin D1 markers of the cell cycle, and triggers a time-dependent increase in DNA fragmentation after release of a thymidine block. Fully differentiated NT2-N cells are forced to enter the mitotic cycle as shown by DNA staining. Chromatin condensation and chromosome formation are initiated, but the cells fail to complete their mitotic cycle. These data suggest that okadaic acid forces differentiated neuronal cells into the mitotic cycle. This pattern of cyclin up-regulation and cell cycle shift is compared with apoptosis induced by neurotrophic factor deprivation in differentiated rat pheochromocytoma PC12 cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Okadaic acid Nuydens, Rony oth De Jong, Mirjam oth Van Den Kieboom, Gerd oth Heers, Cara oth Dispersyn, Gwenda oth Cornelissen, Frans oth Nuyens, Roger oth Borgers, Marcel oth Geerts, Hugo oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 70(1998), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:70 year:1998 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1998.70031124.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 70 1998 3 0 |
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10.1046/j.1471-4159.1998.70031124.x doi (DE-627)NLEJ243163142 DE-627 ger DE-627 rakwb Okadaic Acid-Induced Apoptosis in Neuronal Cells: Evidence for an Abortive Mitotic Attempt Oxford, UK Blackwell Science Ltd 1998 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylation of various proteins, such as the microtubule-associated protein tau. Okadaic acid induces programmed cell death in the human neuroblastoma cell lines TR14 and NT2-N, as evidenced by fragmentation of DNA and attenuation of this process by protein synthesis inhibitors. In differentiated TR14 cells, okadaic acid increases the fraction of cells in the S phase, induces the appearance of cyclin B1 and cyclin D1 markers of the cell cycle, and triggers a time-dependent increase in DNA fragmentation after release of a thymidine block. Fully differentiated NT2-N cells are forced to enter the mitotic cycle as shown by DNA staining. Chromatin condensation and chromosome formation are initiated, but the cells fail to complete their mitotic cycle. These data suggest that okadaic acid forces differentiated neuronal cells into the mitotic cycle. This pattern of cyclin up-regulation and cell cycle shift is compared with apoptosis induced by neurotrophic factor deprivation in differentiated rat pheochromocytoma PC12 cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Okadaic acid Nuydens, Rony oth De Jong, Mirjam oth Van Den Kieboom, Gerd oth Heers, Cara oth Dispersyn, Gwenda oth Cornelissen, Frans oth Nuyens, Roger oth Borgers, Marcel oth Geerts, Hugo oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 70(1998), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:70 year:1998 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1998.70031124.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 70 1998 3 0 |
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10.1046/j.1471-4159.1998.70031124.x doi (DE-627)NLEJ243163142 DE-627 ger DE-627 rakwb Okadaic Acid-Induced Apoptosis in Neuronal Cells: Evidence for an Abortive Mitotic Attempt Oxford, UK Blackwell Science Ltd 1998 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylation of various proteins, such as the microtubule-associated protein tau. Okadaic acid induces programmed cell death in the human neuroblastoma cell lines TR14 and NT2-N, as evidenced by fragmentation of DNA and attenuation of this process by protein synthesis inhibitors. In differentiated TR14 cells, okadaic acid increases the fraction of cells in the S phase, induces the appearance of cyclin B1 and cyclin D1 markers of the cell cycle, and triggers a time-dependent increase in DNA fragmentation after release of a thymidine block. Fully differentiated NT2-N cells are forced to enter the mitotic cycle as shown by DNA staining. Chromatin condensation and chromosome formation are initiated, but the cells fail to complete their mitotic cycle. These data suggest that okadaic acid forces differentiated neuronal cells into the mitotic cycle. This pattern of cyclin up-regulation and cell cycle shift is compared with apoptosis induced by neurotrophic factor deprivation in differentiated rat pheochromocytoma PC12 cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Okadaic acid Nuydens, Rony oth De Jong, Mirjam oth Van Den Kieboom, Gerd oth Heers, Cara oth Dispersyn, Gwenda oth Cornelissen, Frans oth Nuyens, Roger oth Borgers, Marcel oth Geerts, Hugo oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 70(1998), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:70 year:1998 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1998.70031124.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 70 1998 3 0 |
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okadaic acid-induced apoptosis in neuronal cells: evidence for an abortive mitotic attempt |
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Okadaic Acid-Induced Apoptosis in Neuronal Cells: Evidence for an Abortive Mitotic Attempt |
abstract |
Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylation of various proteins, such as the microtubule-associated protein tau. Okadaic acid induces programmed cell death in the human neuroblastoma cell lines TR14 and NT2-N, as evidenced by fragmentation of DNA and attenuation of this process by protein synthesis inhibitors. In differentiated TR14 cells, okadaic acid increases the fraction of cells in the S phase, induces the appearance of cyclin B1 and cyclin D1 markers of the cell cycle, and triggers a time-dependent increase in DNA fragmentation after release of a thymidine block. Fully differentiated NT2-N cells are forced to enter the mitotic cycle as shown by DNA staining. Chromatin condensation and chromosome formation are initiated, but the cells fail to complete their mitotic cycle. These data suggest that okadaic acid forces differentiated neuronal cells into the mitotic cycle. This pattern of cyclin up-regulation and cell cycle shift is compared with apoptosis induced by neurotrophic factor deprivation in differentiated rat pheochromocytoma PC12 cells. |
abstractGer |
Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylation of various proteins, such as the microtubule-associated protein tau. Okadaic acid induces programmed cell death in the human neuroblastoma cell lines TR14 and NT2-N, as evidenced by fragmentation of DNA and attenuation of this process by protein synthesis inhibitors. In differentiated TR14 cells, okadaic acid increases the fraction of cells in the S phase, induces the appearance of cyclin B1 and cyclin D1 markers of the cell cycle, and triggers a time-dependent increase in DNA fragmentation after release of a thymidine block. Fully differentiated NT2-N cells are forced to enter the mitotic cycle as shown by DNA staining. Chromatin condensation and chromosome formation are initiated, but the cells fail to complete their mitotic cycle. These data suggest that okadaic acid forces differentiated neuronal cells into the mitotic cycle. This pattern of cyclin up-regulation and cell cycle shift is compared with apoptosis induced by neurotrophic factor deprivation in differentiated rat pheochromocytoma PC12 cells. |
abstract_unstemmed |
Abstract: There is increasing evidence that apoptosis in postmitotic neurons is associated with a frustrated attempt to reenter the mitotic cycle. Okadaic acid, a specific protein phosphatase inhibitor, is currently used in models of Alzheimer's research to increase the degree of phosphorylation of various proteins, such as the microtubule-associated protein tau. Okadaic acid induces programmed cell death in the human neuroblastoma cell lines TR14 and NT2-N, as evidenced by fragmentation of DNA and attenuation of this process by protein synthesis inhibitors. In differentiated TR14 cells, okadaic acid increases the fraction of cells in the S phase, induces the appearance of cyclin B1 and cyclin D1 markers of the cell cycle, and triggers a time-dependent increase in DNA fragmentation after release of a thymidine block. Fully differentiated NT2-N cells are forced to enter the mitotic cycle as shown by DNA staining. Chromatin condensation and chromosome formation are initiated, but the cells fail to complete their mitotic cycle. These data suggest that okadaic acid forces differentiated neuronal cells into the mitotic cycle. This pattern of cyclin up-regulation and cell cycle shift is compared with apoptosis induced by neurotrophic factor deprivation in differentiated rat pheochromocytoma PC12 cells. |
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Okadaic Acid-Induced Apoptosis in Neuronal Cells: Evidence for an Abortive Mitotic Attempt |
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Nuydens, Rony De Jong, Mirjam Van Den Kieboom, Gerd Heers, Cara Dispersyn, Gwenda Cornelissen, Frans Nuyens, Roger Borgers, Marcel Geerts, Hugo |
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Nuydens, Rony De Jong, Mirjam Van Den Kieboom, Gerd Heers, Cara Dispersyn, Gwenda Cornelissen, Frans Nuyens, Roger Borgers, Marcel Geerts, Hugo |
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