The Experts below are selected from a list of 6495 Experts worldwide ranked by ideXlab platform
David C Pallas - One of the best experts on this subject based on the ideXlab platform.
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Tumor suppressor WARTS ensures genomic integrity by regulating both mitotic progression and G_1 Tetraploidy checkpoint function
Oncogene, 2004Co-Authors: Shin-ichi Iida, Toru Hirota, Tetsuro Morisaki, Tomotoshi Marumoto, Toshihiro Hara, Shinji Kuninaka, Shinobu Honda, Ken-ichiro Kosai, Michio Kawasuji, David C PallasAbstract:Defects in chromosomes or mitotic spindles activate the spindle checkpoint, resulting in cell cycle arrest at prometaphase. The prolonged activation of spindle checkpoint generally leads to mitotic exit without segregation after a transient mitotic arrest and the consequent formation of tetraploid G_1 cells. These tetraploid cells are usually blocked to enter the subsequent S phase by the activation of p53/pRb pathway, which is referred to as the G_1 Tetraploidy checkpoint. A human homologue of the Drosophila warts tumor suppressor, WARTS, is an evolutionarily conserved serine–threonine kinase and implicated in development of human tumors. We previously showed that WARTS plays a crucial role in controlling mitotic progression by forming a regulatory complex with zyxin, a regulator of actin filament assembly, on mitotic apparatus. However, when WARTS is activated during cell cycle and how the loss of WARTS function leads to tumorigenesis have not been elucidated. Here we show that WARTS is activated during mitosis in mammalian cells, and that overexpression of a kinase-inactive WARTS in Rat1 fibroblasts significantly induced mitotic delay. This delay resulted from prolonged activation of the spindle assembly checkpoint and was frequently followed by mitotic slippage and the development of Tetraploidy. The resulting tetraploid cells then abrogated the G_1 Tetraploidy checkpoint and entered S phase to achieve a DNA content of 8N. This impairment of G_1 Tetraploidy checkpoint was caused as a consequence of failure to induce p53 expression by expressing a kinase-inactive WARTS. WARTS thus plays a critical role in maintenance of ploidy through its actions in both mitotic progression and the G_1 Tetraploidy checkpoint.
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Tumor suppressor WARTS ensures genomic integrity by regulating both mitotic progression and G1 Tetraploidy checkpoint function.
Oncogene, 2004Co-Authors: Shin-ichi Iida, Toru Hirota, Tetsuro Morisaki, Tomotoshi Marumoto, Toshihiro Hara, Shinji Kuninaka, Shinobu Honda, Ken-ichiro Kosai, Michio Kawasuji, David C PallasAbstract:Defects in chromosomes or mitotic spindles activate the spindle checkpoint, resulting in cell cycle arrest at prometaphase. The prolonged activation of spindle checkpoint generally leads to mitotic exit without segregation after a transient mitotic arrest and the consequent formation of tetraploid G(1) cells. These tetraploid cells are usually blocked to enter the subsequent S phase by the activation of p53/pRb pathway, which is referred to as the G(1) Tetraploidy checkpoint. A human homologue of the Drosophila warts tumor suppressor, WARTS, is an evolutionarily conserved serine-threonine kinase and implicated in development of human tumors. We previously showed that WARTS plays a crucial role in controlling mitotic progression by forming a regulatory complex with zyxin, a regulator of actin filament assembly, on mitotic apparatus. However, when WARTS is activated during cell cycle and how the loss of WARTS function leads to tumorigenesis have not been elucidated. Here we show that WARTS is activated during mitosis in mammalian cells, and that overexpression of a kinase-inactive WARTS in Rat1 fibroblasts significantly induced mitotic delay. This delay resulted from prolonged activation of the spindle assembly checkpoint and was frequently followed by mitotic slippage and the development of Tetraploidy. The resulting tetraploid cells then abrogated the G(1) Tetraploidy checkpoint and entered S phase to achieve a DNA content of 8N. This impairment of G(1) Tetraploidy checkpoint was caused as a consequence of failure to induce p53 expression by expressing a kinase-inactive WARTS. WARTS thus plays a critical role in maintenance of ploidy through its actions in both mitotic progression and the G(1) Tetraploidy checkpoint.
Shin-ichi Iida - One of the best experts on this subject based on the ideXlab platform.
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Tumor suppressor WARTS ensures genomic integrity by regulating both mitotic progression and G_1 Tetraploidy checkpoint function
Oncogene, 2004Co-Authors: Shin-ichi Iida, Toru Hirota, Tetsuro Morisaki, Tomotoshi Marumoto, Toshihiro Hara, Shinji Kuninaka, Shinobu Honda, Ken-ichiro Kosai, Michio Kawasuji, David C PallasAbstract:Defects in chromosomes or mitotic spindles activate the spindle checkpoint, resulting in cell cycle arrest at prometaphase. The prolonged activation of spindle checkpoint generally leads to mitotic exit without segregation after a transient mitotic arrest and the consequent formation of tetraploid G_1 cells. These tetraploid cells are usually blocked to enter the subsequent S phase by the activation of p53/pRb pathway, which is referred to as the G_1 Tetraploidy checkpoint. A human homologue of the Drosophila warts tumor suppressor, WARTS, is an evolutionarily conserved serine–threonine kinase and implicated in development of human tumors. We previously showed that WARTS plays a crucial role in controlling mitotic progression by forming a regulatory complex with zyxin, a regulator of actin filament assembly, on mitotic apparatus. However, when WARTS is activated during cell cycle and how the loss of WARTS function leads to tumorigenesis have not been elucidated. Here we show that WARTS is activated during mitosis in mammalian cells, and that overexpression of a kinase-inactive WARTS in Rat1 fibroblasts significantly induced mitotic delay. This delay resulted from prolonged activation of the spindle assembly checkpoint and was frequently followed by mitotic slippage and the development of Tetraploidy. The resulting tetraploid cells then abrogated the G_1 Tetraploidy checkpoint and entered S phase to achieve a DNA content of 8N. This impairment of G_1 Tetraploidy checkpoint was caused as a consequence of failure to induce p53 expression by expressing a kinase-inactive WARTS. WARTS thus plays a critical role in maintenance of ploidy through its actions in both mitotic progression and the G_1 Tetraploidy checkpoint.
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Tumor suppressor WARTS ensures genomic integrity by regulating both mitotic progression and G1 Tetraploidy checkpoint function.
Oncogene, 2004Co-Authors: Shin-ichi Iida, Toru Hirota, Tetsuro Morisaki, Tomotoshi Marumoto, Toshihiro Hara, Shinji Kuninaka, Shinobu Honda, Ken-ichiro Kosai, Michio Kawasuji, David C PallasAbstract:Defects in chromosomes or mitotic spindles activate the spindle checkpoint, resulting in cell cycle arrest at prometaphase. The prolonged activation of spindle checkpoint generally leads to mitotic exit without segregation after a transient mitotic arrest and the consequent formation of tetraploid G(1) cells. These tetraploid cells are usually blocked to enter the subsequent S phase by the activation of p53/pRb pathway, which is referred to as the G(1) Tetraploidy checkpoint. A human homologue of the Drosophila warts tumor suppressor, WARTS, is an evolutionarily conserved serine-threonine kinase and implicated in development of human tumors. We previously showed that WARTS plays a crucial role in controlling mitotic progression by forming a regulatory complex with zyxin, a regulator of actin filament assembly, on mitotic apparatus. However, when WARTS is activated during cell cycle and how the loss of WARTS function leads to tumorigenesis have not been elucidated. Here we show that WARTS is activated during mitosis in mammalian cells, and that overexpression of a kinase-inactive WARTS in Rat1 fibroblasts significantly induced mitotic delay. This delay resulted from prolonged activation of the spindle assembly checkpoint and was frequently followed by mitotic slippage and the development of Tetraploidy. The resulting tetraploid cells then abrogated the G(1) Tetraploidy checkpoint and entered S phase to achieve a DNA content of 8N. This impairment of G(1) Tetraploidy checkpoint was caused as a consequence of failure to induce p53 expression by expressing a kinase-inactive WARTS. WARTS thus plays a critical role in maintenance of ploidy through its actions in both mitotic progression and the G(1) Tetraploidy checkpoint.
Daniel Cohen - One of the best experts on this subject based on the ideXlab platform.
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in vitro chromosome doubling of nine zantedeschia cultivars
Plant Cell Tissue and Organ Culture, 1996Co-Authors: Daniel CohenAbstract:Tetraploid plants have been produced from nineZantedeschia cultivars usingin vitro colchicine treatment. Rapidly-multiplying shoot cultures were treated on a medium containing 0.05% colchicine for 1, 2 or 4 days to induce chromosome doubling. Following the treatment, most shoots were killed but the surviving shoots were multiplied for several subcultures. These shoots were then rootedin vitro and transferred to a greenhouse. Plants were screened 2 months later by measuring stomatal length, and 110 out of 565 plants were selected as putative tetraploids with a stomatal length significantly greater than in diploid control plants. Chromosome counts were carried out on root tips from 44 plants and confirmed that 38 were tetraploids, 2 were chimeras (predominantly tetraploid with a few octoploid cells), and 4 were diploids. Stomatal length has been rechecked in mature tetraploid plants of the cultivar Black Magic, demonstrating that stomatal length is a good indicator of ploidy level inZantedeschia. This study has shown that multiplying colchicine-treated shootsin vitro for several subcultures prior to transfer to soil produced very few chimeras. The stomatal length measurements are non-destructive and allow the rapid screening of a population for tetraploids.
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In vitro chromosome doubling of nineZantedeschia cultivars
Plant Cell Tissue and Organ Culture, 1996Co-Authors: Daniel Cohen, Daniel CohenAbstract:Tetraploid plants have been produced from nine Zantedeschia cultivars using in vitro colchicine treatment. Rapidly-multiplying shoot cultures were treated on a medium containing 0.05% colchicine for 1, 2 or 4 days to induce chromosome doubling. Following the treatment, most shoots were killed but the surviving shoots were multiplied for several subcultures. These shoots were then rooted in vitro and transferred to a greenhouse. Plants were screened 2 months later by measuring stomatal length, and 110 out of 565 plants were selected as putative tetraploids with a stomatal length significantly greater than in diploid control plants. Chromosome counts were carried out on root tips from 44 plants and confirmed that 38 were tetraploids, 2 were chimeras (predominantly tetraploid with a few octoploid cells), and 4 were diploids. Stomatal length has been rechecked in mature tetraploid plants of the cultivar Black Magic, demonstrating that stomatal length is a good indicator of ploidy level in Zantedeschia . This study has shown that multiplying colchicine-treated shoots in vitro for several subcultures prior to transfer to soil produced very few chimeras. The stomatal length measurements are non-destructive and allow the rapid screening of a population for tetraploids.
Ken-ichiro Kosai - One of the best experts on this subject based on the ideXlab platform.
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Tumor suppressor WARTS ensures genomic integrity by regulating both mitotic progression and G_1 Tetraploidy checkpoint function
Oncogene, 2004Co-Authors: Shin-ichi Iida, Toru Hirota, Tetsuro Morisaki, Tomotoshi Marumoto, Toshihiro Hara, Shinji Kuninaka, Shinobu Honda, Ken-ichiro Kosai, Michio Kawasuji, David C PallasAbstract:Defects in chromosomes or mitotic spindles activate the spindle checkpoint, resulting in cell cycle arrest at prometaphase. The prolonged activation of spindle checkpoint generally leads to mitotic exit without segregation after a transient mitotic arrest and the consequent formation of tetraploid G_1 cells. These tetraploid cells are usually blocked to enter the subsequent S phase by the activation of p53/pRb pathway, which is referred to as the G_1 Tetraploidy checkpoint. A human homologue of the Drosophila warts tumor suppressor, WARTS, is an evolutionarily conserved serine–threonine kinase and implicated in development of human tumors. We previously showed that WARTS plays a crucial role in controlling mitotic progression by forming a regulatory complex with zyxin, a regulator of actin filament assembly, on mitotic apparatus. However, when WARTS is activated during cell cycle and how the loss of WARTS function leads to tumorigenesis have not been elucidated. Here we show that WARTS is activated during mitosis in mammalian cells, and that overexpression of a kinase-inactive WARTS in Rat1 fibroblasts significantly induced mitotic delay. This delay resulted from prolonged activation of the spindle assembly checkpoint and was frequently followed by mitotic slippage and the development of Tetraploidy. The resulting tetraploid cells then abrogated the G_1 Tetraploidy checkpoint and entered S phase to achieve a DNA content of 8N. This impairment of G_1 Tetraploidy checkpoint was caused as a consequence of failure to induce p53 expression by expressing a kinase-inactive WARTS. WARTS thus plays a critical role in maintenance of ploidy through its actions in both mitotic progression and the G_1 Tetraploidy checkpoint.
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Tumor suppressor WARTS ensures genomic integrity by regulating both mitotic progression and G1 Tetraploidy checkpoint function.
Oncogene, 2004Co-Authors: Shin-ichi Iida, Toru Hirota, Tetsuro Morisaki, Tomotoshi Marumoto, Toshihiro Hara, Shinji Kuninaka, Shinobu Honda, Ken-ichiro Kosai, Michio Kawasuji, David C PallasAbstract:Defects in chromosomes or mitotic spindles activate the spindle checkpoint, resulting in cell cycle arrest at prometaphase. The prolonged activation of spindle checkpoint generally leads to mitotic exit without segregation after a transient mitotic arrest and the consequent formation of tetraploid G(1) cells. These tetraploid cells are usually blocked to enter the subsequent S phase by the activation of p53/pRb pathway, which is referred to as the G(1) Tetraploidy checkpoint. A human homologue of the Drosophila warts tumor suppressor, WARTS, is an evolutionarily conserved serine-threonine kinase and implicated in development of human tumors. We previously showed that WARTS plays a crucial role in controlling mitotic progression by forming a regulatory complex with zyxin, a regulator of actin filament assembly, on mitotic apparatus. However, when WARTS is activated during cell cycle and how the loss of WARTS function leads to tumorigenesis have not been elucidated. Here we show that WARTS is activated during mitosis in mammalian cells, and that overexpression of a kinase-inactive WARTS in Rat1 fibroblasts significantly induced mitotic delay. This delay resulted from prolonged activation of the spindle assembly checkpoint and was frequently followed by mitotic slippage and the development of Tetraploidy. The resulting tetraploid cells then abrogated the G(1) Tetraploidy checkpoint and entered S phase to achieve a DNA content of 8N. This impairment of G(1) Tetraploidy checkpoint was caused as a consequence of failure to induce p53 expression by expressing a kinase-inactive WARTS. WARTS thus plays a critical role in maintenance of ploidy through its actions in both mitotic progression and the G(1) Tetraploidy checkpoint.
Michio Kawasuji - One of the best experts on this subject based on the ideXlab platform.
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Tumor suppressor WARTS ensures genomic integrity by regulating both mitotic progression and G_1 Tetraploidy checkpoint function
Oncogene, 2004Co-Authors: Shin-ichi Iida, Toru Hirota, Tetsuro Morisaki, Tomotoshi Marumoto, Toshihiro Hara, Shinji Kuninaka, Shinobu Honda, Ken-ichiro Kosai, Michio Kawasuji, David C PallasAbstract:Defects in chromosomes or mitotic spindles activate the spindle checkpoint, resulting in cell cycle arrest at prometaphase. The prolonged activation of spindle checkpoint generally leads to mitotic exit without segregation after a transient mitotic arrest and the consequent formation of tetraploid G_1 cells. These tetraploid cells are usually blocked to enter the subsequent S phase by the activation of p53/pRb pathway, which is referred to as the G_1 Tetraploidy checkpoint. A human homologue of the Drosophila warts tumor suppressor, WARTS, is an evolutionarily conserved serine–threonine kinase and implicated in development of human tumors. We previously showed that WARTS plays a crucial role in controlling mitotic progression by forming a regulatory complex with zyxin, a regulator of actin filament assembly, on mitotic apparatus. However, when WARTS is activated during cell cycle and how the loss of WARTS function leads to tumorigenesis have not been elucidated. Here we show that WARTS is activated during mitosis in mammalian cells, and that overexpression of a kinase-inactive WARTS in Rat1 fibroblasts significantly induced mitotic delay. This delay resulted from prolonged activation of the spindle assembly checkpoint and was frequently followed by mitotic slippage and the development of Tetraploidy. The resulting tetraploid cells then abrogated the G_1 Tetraploidy checkpoint and entered S phase to achieve a DNA content of 8N. This impairment of G_1 Tetraploidy checkpoint was caused as a consequence of failure to induce p53 expression by expressing a kinase-inactive WARTS. WARTS thus plays a critical role in maintenance of ploidy through its actions in both mitotic progression and the G_1 Tetraploidy checkpoint.
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Tumor suppressor WARTS ensures genomic integrity by regulating both mitotic progression and G1 Tetraploidy checkpoint function.
Oncogene, 2004Co-Authors: Shin-ichi Iida, Toru Hirota, Tetsuro Morisaki, Tomotoshi Marumoto, Toshihiro Hara, Shinji Kuninaka, Shinobu Honda, Ken-ichiro Kosai, Michio Kawasuji, David C PallasAbstract:Defects in chromosomes or mitotic spindles activate the spindle checkpoint, resulting in cell cycle arrest at prometaphase. The prolonged activation of spindle checkpoint generally leads to mitotic exit without segregation after a transient mitotic arrest and the consequent formation of tetraploid G(1) cells. These tetraploid cells are usually blocked to enter the subsequent S phase by the activation of p53/pRb pathway, which is referred to as the G(1) Tetraploidy checkpoint. A human homologue of the Drosophila warts tumor suppressor, WARTS, is an evolutionarily conserved serine-threonine kinase and implicated in development of human tumors. We previously showed that WARTS plays a crucial role in controlling mitotic progression by forming a regulatory complex with zyxin, a regulator of actin filament assembly, on mitotic apparatus. However, when WARTS is activated during cell cycle and how the loss of WARTS function leads to tumorigenesis have not been elucidated. Here we show that WARTS is activated during mitosis in mammalian cells, and that overexpression of a kinase-inactive WARTS in Rat1 fibroblasts significantly induced mitotic delay. This delay resulted from prolonged activation of the spindle assembly checkpoint and was frequently followed by mitotic slippage and the development of Tetraploidy. The resulting tetraploid cells then abrogated the G(1) Tetraploidy checkpoint and entered S phase to achieve a DNA content of 8N. This impairment of G(1) Tetraploidy checkpoint was caused as a consequence of failure to induce p53 expression by expressing a kinase-inactive WARTS. WARTS thus plays a critical role in maintenance of ploidy through its actions in both mitotic progression and the G(1) Tetraploidy checkpoint.
