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Our data suggest that ROS may trigger death of T cells offering an explanation for protection from autoimmunity.
This suggests that ROS may trigger death of virus-specific CD8+ T cells, a phenomenon typically observed during T-cell exhaustion.
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Loss or malfunction of key biomolecules may even trigger death of cells depending on the duration and intensity of stress.
But the study does support the idea that particular gene variants coupled with certain stresses may trigger sudden death.
Insufficient degradation due to altered protein structure or proteasome inhibition may trigger cell death.
Further, the stimulation of G protein-coupled P2Y receptors may trigger cell death by promoting the release of glutamate from nerve terminals and/or astrocytes [22] shown in vivo or by the activation of early apoptotic enzymes e.g., active caspase 3 via P2Y1 receptors [23].
The accumulation of chlorophyll breakdown products may trigger cell death [ 122].
However, it may trigger cell death if the ER stress is severe.
We also investigated whether CDKL5 expression may trigger cell death in neuroblastoma cells.
Taken together, this work presents first evidence demonstrating that intracellular GSSG may trigger cell death.
GSSG is a functionally active byproduct of GSH metabolism that, under appropriate conditions, may trigger cell death.
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