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Greenfield Sluder - One of the best experts on this subject based on the ideXlab platform.
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Activation of the apoptotic pathway during prolonged prometaphase blocks daughter cell proliferation
Molecular Biology of the Cell, 2018Co-Authors: Yumi Uetake, Greenfield SluderAbstract:When untransformed human cells spend >1.5 h in prometaphase under standard culture conditions, all daughters arrest in G1 despite normal division of their mothers. We investigate what happens during prolonged prometaphase that leads to daughter cell arrest in the absence of DNA damage. We find that progressive loss of anti-apoptotic MCL-1 Activity and oxidative Stress Act in concert to partially Activate the apoptosis pathway, resulting in the delayed death of some daughters and senescence for the rest. At physiological oxygen levels, longer prometaphase durations are needed for all daughters to arrest. Partial Activation of apoptosis during prolonged prometaphase leads to persistent caspase Activity, which Activates the kinase cascade mediating the post-mitotic Activation of p38. This in turn Activates p53, and the consequent expression of p21stops the cell cycle. This mechanism can prevent cells suffering intrActable mitotic defects, which modestly prolong mitosis but allow its completion without DNA damage, from producing future cell generations that are susceptible to the evolution of a transformed phenotype.
Yumi Uetake - One of the best experts on this subject based on the ideXlab platform.
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Activation of the apoptotic pathway during prolonged prometaphase blocks daughter cell proliferation
Molecular Biology of the Cell, 2018Co-Authors: Yumi Uetake, Greenfield SluderAbstract:When untransformed human cells spend >1.5 h in prometaphase under standard culture conditions, all daughters arrest in G1 despite normal division of their mothers. We investigate what happens during prolonged prometaphase that leads to daughter cell arrest in the absence of DNA damage. We find that progressive loss of anti-apoptotic MCL-1 Activity and oxidative Stress Act in concert to partially Activate the apoptosis pathway, resulting in the delayed death of some daughters and senescence for the rest. At physiological oxygen levels, longer prometaphase durations are needed for all daughters to arrest. Partial Activation of apoptosis during prolonged prometaphase leads to persistent caspase Activity, which Activates the kinase cascade mediating the post-mitotic Activation of p38. This in turn Activates p53, and the consequent expression of p21stops the cell cycle. This mechanism can prevent cells suffering intrActable mitotic defects, which modestly prolong mitosis but allow its completion without DNA damage, from producing future cell generations that are susceptible to the evolution of a transformed phenotype.
Sluder Greenfield - One of the best experts on this subject based on the ideXlab platform.
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Activation of the apoptotic pathway during prolonged prometaphase blocks daughter cell proliferation
eScholarship@UMMS, 2018Co-Authors: Uetake Yumi, Sluder GreenfieldAbstract:When untransformed human cells spend \u3e1.5 hr. in prometaphase under standard culture conditions, all daughters arrest in G1 despite normal division of their mothers. We investigate what happens during prolonged prometaphase that leads to daughter cell arrest in the absence of DNA damage. We find that progressive loss of anti-apoptotic MCL-1 Activity and oxidative Stress Act in concert to partially Activate the apoptosis pathway resulting in the delayed death of some daughters and senescence for the rest. At physiological oxygen levels, longer prometaphase durations are needed for all daughters to arrest. Partial Activation of apoptosis during prolonged prometaphase leads to persistent caspase Activity, which Activates the kinase cascade mediating the post mitotic Activation of p38. This in turn Activates p53 and the consequent expression of p21stops the cell cycle. This mechanism can prevent cells suffering intrActable mitotic defects, which modestly prolong mitosis but allow its completion without DNA damage, from producing future cell generations that are susceptible to the evolution of a transformed phenotype
Uetake Yumi - One of the best experts on this subject based on the ideXlab platform.
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Activation of the apoptotic pathway during prolonged prometaphase blocks daughter cell proliferation
eScholarship@UMMS, 2018Co-Authors: Uetake Yumi, Sluder GreenfieldAbstract:When untransformed human cells spend \u3e1.5 hr. in prometaphase under standard culture conditions, all daughters arrest in G1 despite normal division of their mothers. We investigate what happens during prolonged prometaphase that leads to daughter cell arrest in the absence of DNA damage. We find that progressive loss of anti-apoptotic MCL-1 Activity and oxidative Stress Act in concert to partially Activate the apoptosis pathway resulting in the delayed death of some daughters and senescence for the rest. At physiological oxygen levels, longer prometaphase durations are needed for all daughters to arrest. Partial Activation of apoptosis during prolonged prometaphase leads to persistent caspase Activity, which Activates the kinase cascade mediating the post mitotic Activation of p38. This in turn Activates p53 and the consequent expression of p21stops the cell cycle. This mechanism can prevent cells suffering intrActable mitotic defects, which modestly prolong mitosis but allow its completion without DNA damage, from producing future cell generations that are susceptible to the evolution of a transformed phenotype
Umu Ozca - One of the best experts on this subject based on the ideXlab platform.
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endoplasmic reticulum Stress plays a central role in development of leptin resistance
Cell Metabolism, 2009Co-Authors: Lale Ozca, Ayse Seda Ergi, Jaso Chung, Sumi Sarka, Duyu Nie, Marti G Myers, Umu OzcaAbstract:Leptin has not evolved as a therapeutic modality for the treatment of obesity due to the prevalence of leptin resistance in a majority of the obese population. Nevertheless, the molecular mechanisms of leptin resistance remain poorly understood. Here, we show that increased endoplasmic reticulum (ER) Stress and Activation of the unfolded protein response (UPR) in the hypothalamus of obese mice inhibits leptin receptor signaling. The genetic imposition of reduced ER capacity in mice results in severe leptin resistance and leads to a significant augmentation of obesity on a high-fat diet. Moreover, we show that chemical chaperones, 4-phenyl butyric acid (PBA), and tauroursodeoxycholic acid (TUDCA), which have the ability to decrease ER Stress, Act as leptin-sensitizing agents. Taken together, our results may provide the basis for a novel treatment of obesity.