Now showing items 1-6 of 6
Nerve growth factor-mediated inhibition of apoptosis post-caspase activation is due to removal of active caspase-3 in a lysosome-dependent manner
(Nature Publishing Group, 2014-05-01)
Nerve growth factor (NGF) is well characterised as an important pro-survival factor in neuronal cells that can inhibit apoptotic cell death upstream of mitochondrial outer membrane permeabilisation. Here we addressed the ...
The integrated stress response
(EMBO Press, 2016-09-14)
In response to diverse stress stimuli, eukaryotic cells activate a common adaptive pathway, termed the integrated stress response (ISR), to restore cellular homeostasis. The core event in this pathway is the phosphorylation ...
HSP72 Protects Cells from ER Stress-induced Apoptosis via Enhancement of IRE1¿-XBP1 Signaling through a Physical Interaction
Endoplasmic reticulum (ER) stress is a feature of secretory cells and of many diseases including cancer, neurodegeneration, and diabetes. Adaptation to ER stress depends on the activation of a signal transduction pathway ...
Mechanisms of ER Stress-Mediated Mitochondrial Membrane Permeabilization
During apoptosis, the process of mitochondrial outer membrane permeabilization (MOMP) represents a point-of-no-return as it commits the cell to death. Here we have assessed the role of caspases, Bcl-2 family members and ...
Methods for Monitoring Endoplasmic Reticulum Stress and the Unfolded Protein Response
The endoplasmic reticulum (ER) is the site of folding of membrane and secreted proteins in the cell. Physiological or pathological processes that disturb protein folding in the endoplasmic reticulum cause ER stress and ...
Rapid and efficient cancer cell killing mediated by high-affinity death receptor homotrimerizing TRAIL variants
(Macmillan Publishers Limited, 2010)
The tumour necrosis factor family member TNF-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in a variety of cancer cells through the activation of death receptors 4 (DR4) and 5 (DR5) and is considered ...