Molecular Regulation of Cell-Cycle Progression and Apoptosis in Mammalian Cells: Implications for Biotechnology

Fussenegger, Martin; Bailey, James E.

doi:10.1021/bp9800891

Cited by 108 publications

(64 citation statements)

References 230 publications

(350 reference statements)

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“…125 Accumulating evidence indicates that the microtubule network integrates mechanistic components of both the cell cycle and apoptosis. 59,126,127 Therefore, it is not surprising that paclitaxel has multiple effects on modulation of both the cell cycle and apoptosis, which account for its killing of cancer cells. Further elucidation of the mechanisms of paclitaxel-initiated apoptosis will help us to develop better taxane-based regimens for cancer therapy.…”

Section: Discussionmentioning

confidence: 99%

Paclitaxel-induced cell death

Wang

Soong

2000

Cancer

563

185

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Section: Discussionmentioning

confidence: 99%

Paclitaxel-induced cell death

Wang

Soong

2000

Cancer

563

185

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“…These results indicate that Tat-NOL3 inhibits ROS-induced DNA fragmentation in HT22 cells. The activation of p53 by elevated ROS levels elicits cell cycle arrest or apoptosis (40). Oxidative DNA damage, which may result in DNA fragmentation causing cells to undergo cycle arrest followed by apoptotic cell death (38).…”

Section: Tat-nol3 Protein Increases Cell Viability and Inhibits Ros-imentioning

confidence: 99%

Tat-NOL3 protects against hippocampal neuronal cell death induced by oxidative stress through the regulation of apoptotic pathways

Sohn

Shin

Eum

et al. 2016

International Journal of Molecular Medicine

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Abstract. Oxidative stress-induced apoptosis is associated with neuronal cell death and ischemia. The NOL3 [nucleolar protein 3 (apoptosis repressor with CARD domain)] protein protects against oxidative stress-induced cell death. However, the protective mechanism responsible for this effect as well as the effects of NOL3 against oxidative stress in ischemia remain unclear. Thus, we examined the protective effects of NOL3 protein on hydrogen peroxide (H 2 O 2 )-induced oxidative stress and the mechanism responsible for these effects in hippocampal neuronal HT22 cells and in an animal model of forebrain ischemia using Tat-fused NOL3 protein (Tat-NOL3). Purified Tat-NOL3 protein transduced into the H 2 O 2 -exposed HT22 cells and inhibited the production of reactive oxygen species (ROS), DNA fragmentation and reduced mitochondrial membrane potential (Δ Ψm ). In addition, Tat-NOL3 prevented neuronal cell death through the regulation of apoptotic signaling pathways including Bax, Bcl-2, caspase-2, -3 and -8, PARP and p53. In addition, Tat-NOL3 protein transduced into the animal brains and significantly protected against neuronal cell death in the CA1 region of the hippocampus by regulating the activation of microglia and astrocytes. Taken together, these findings demonstrate that Tat-NOL3 protein protects against oxidative stress-induced neuronal cell death by regulating oxidative stress and by acting as an anti-apoptotic protein. Thus, we suggest that Tat-NOL3 represents a potential therapeutic agent for protection against ischemic brain injury.

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“…A more thorough review on cell cycle progression in mammalian cells can be found in (Fussenegger and Bailey, 1998). A study on the population distribution of hybridoma cells during perfusion was carried out by flow cyometric analysis (Park and Ryu, 1994).…”

Section: Cell Cyclementioning

confidence: 99%