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Upon ligand binding, integrins may trigger cells to secrete growth factors and/or cytokines, which in turn can bind to their receptors in an autocrine or paracrine manner to induce further signaling.
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Insufficient degradation due to altered protein structure or proteasome inhibition may trigger cell death.
Furthermore, we hypothesize that, like in the solid tumors mentioned above, AQP5 may trigger cell proliferation in leukemic cells.
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].
These described changes may trigger cell damage and death.
We also investigated whether CDKL5 expression may trigger cell death in neuroblastoma cells.
It is conceivable that the p21/cyclin D interval variations may trigger cell cycle progression.
The accumulation of chlorophyll breakdown products may trigger cell death [ 122].
However, it may trigger cell death if the ER stress is severe.
50 Therefore, p53 or cellular senescence may trigger cell competition and establish ONCs.
Taken together, this work presents first evidence demonstrating that intracellular GSSG may trigger cell death.
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