Besides mediating apoptosis, TNFα induces the canonical NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) pathway triggering the expression of genes involved in inflammation, immunity, cell migration and cell survival (Gyrd-Hansen & Meier, 2010).
In fact, using BH3 profiling and videomicroscopy, we describe a genuine switch in cell death pathways triggered during metaphase-arrested cells that mainly depends on Bcl-xL.
Additionally, different ligands and receptors are subject to regulation by other cell signaling pathways triggered by a variety of stimuli (Kopan and Ilagan, 2009).
Cell death pathways triggered by DNA damage can be regulated by CK2 involving the phosphorylation of XRCC1.
Since the therapeutic goal of most anticancer drugs is to induce tumor-selective apoptosis, it is critical to understand the specific cell death pathways triggered by drugs.
The molecular cell death pathways triggered by the critical DNA lesions are not predictable and appear to be dependent on the cellular background.
Generation of mitochondria-derived oxidative free radicals has been implicated in the cell necrotic pathways triggered by cytotoxic agents, and we sought to examine its role in hypoxic necrosis.
According to this study, cell death signaling pathways triggered by anti-GD2 mAbs are complex and could be attributed to non-classical mechanisms of cell death, with features of apoptosis (e.g. AVD) and necrosis (e.g. plasma membrane permeability), and with involvement of mitochondria-dependent pathways.
The necroptotic cell death pathway triggered by TNF in cells with elevated RIPK3 did not require the presence of FADD, RIPK1, caspase 8, or Bax/Bak.
The implementation of gene expression studies in isolated cell populations to identify pathways triggered in these different models will be instrumental in determining the molecular events that define prion pathogenesis in vivo.
