<p>Oxidative stress in dying cells is likely of mitochondrial origin and results in highly toxic JNK. However, low levels of ROS propagate to adjacent surviving cells (arrows). Non-deleterious ROS will activate moderate levels of JNK and p38 only in surviving cells. P38 and JNK are required for cytokine activation and tissue repair.</p
The temporal contribution of varying cell death pathways induced by oxidative stress and the mechani...
Many primary tumors as well as transformed cell lines display high sensitivity to chemotherapeutic d...
AbstractTo clarify the relationship between reactive oxygen species (ROS) and cell death during isch...
Upon apoptotic stimuli, epithelial cells compensate the gaps left by dead cells by activating prolif...
SummaryProinflammatory cytokine TNFα triggers cell death by inducing reactive oxygen species (ROS). ...
<div><p>Upon apoptotic stimuli, epithelial cells compensate the gaps left by dead cells by activatin...
International audienceDuring apoptosis, mitochondrial membrane permeability (MMP) increases and the ...
The production of reactive oxygen species is a normal part of cell physiology, but many internal and...
Upon apoptotic stimuli, epithelial cells compensate the gaps left by dead cells by activating prolif...
SummaryTNFα is a pleiotropic cytokine that induces either cell proliferation or cell death. Inhibiti...
Reactive oxygen species (ROS) are produced as a by-product of cellular metabolic pathways and functi...
Reperfusion injury occurs when oxygenated blood is returned to previously ischemic tissue. It involv...
ROS are diverse and abundant in biological systems. While excessive ROS production clearly damages D...
The c-Jun NH(2)-terminal kinase (JNK) has been implicated in both cell death and survival responses ...
Reactive oxygen species (ROS) are a family of small but highly reactive molecules. Although it has b...
The temporal contribution of varying cell death pathways induced by oxidative stress and the mechani...
Many primary tumors as well as transformed cell lines display high sensitivity to chemotherapeutic d...
AbstractTo clarify the relationship between reactive oxygen species (ROS) and cell death during isch...
Upon apoptotic stimuli, epithelial cells compensate the gaps left by dead cells by activating prolif...
SummaryProinflammatory cytokine TNFα triggers cell death by inducing reactive oxygen species (ROS). ...
<div><p>Upon apoptotic stimuli, epithelial cells compensate the gaps left by dead cells by activatin...
International audienceDuring apoptosis, mitochondrial membrane permeability (MMP) increases and the ...
The production of reactive oxygen species is a normal part of cell physiology, but many internal and...
Upon apoptotic stimuli, epithelial cells compensate the gaps left by dead cells by activating prolif...
SummaryTNFα is a pleiotropic cytokine that induces either cell proliferation or cell death. Inhibiti...
Reactive oxygen species (ROS) are produced as a by-product of cellular metabolic pathways and functi...
Reperfusion injury occurs when oxygenated blood is returned to previously ischemic tissue. It involv...
ROS are diverse and abundant in biological systems. While excessive ROS production clearly damages D...
The c-Jun NH(2)-terminal kinase (JNK) has been implicated in both cell death and survival responses ...
Reactive oxygen species (ROS) are a family of small but highly reactive molecules. Although it has b...
The temporal contribution of varying cell death pathways induced by oxidative stress and the mechani...
Many primary tumors as well as transformed cell lines display high sensitivity to chemotherapeutic d...
AbstractTo clarify the relationship between reactive oxygen species (ROS) and cell death during isch...