RT Journal Article
T1 Detecting Autophagy in Response to ER Stress Signals in Cancer
A1 Salazar Roa, María
A1 Hernández Tiedra, Sonia
A1 Torres, Sofía
A1 Lorente Pérez, María Del Mar
A1 Guzmán Pastor, Manuel
A1 Velasco Díez, Guillermo
AB Different physiological and pathological situations that produce alterations in the endoplasmic reticulum, lead to a condition known as ER stress. ER stress activates a complex intracellular signal transduction pathway, called unfolded protein response (UPR). UPR is tailored essentially to reestablish ER homeostasis. However, when persistent, ER stress can switch the cytoprotective functions of UPR into cell death promoting mechanisms. One of the cellular mechanisms that are regulated by ER stress is autophagy. Autophagy is a cellular process by which different cytoplasmic components including organelles are targeted for degradation to the autophagosomes. Interestingly, like ER stress, autophagy can be a protective or a cell death promoting mechanism. Recently, a variety of anticancer therapies (including those that stimulate ER stress) have been shown to activate autophagy in tumor cells, which has been proposed to either enhance cancer cell death or act as a mechanism of resistance to chemotherapy.In this chapter, we will describe some of the procedures that are currently used to analyze autophagy as well as some of the experimental approaches that can be undertaken to investigate the connection between ER stress and autophagy in cancer.
PB Elsevier
SN 0076-6879
YR 2011
FD 2011
LK https://hdl.handle.net/20.500.14352/125736
UL https://hdl.handle.net/20.500.14352/125736
LA eng
NO Salazar, M., Hernández-Tiedra, S., Torres, S., Lorente, M., Guzmán, M., & Velasco, G. (2011). Detecting autophagy in response to ER stress signals in cancer. En Methods in Enzymology (Vol. 489, Número C, pp. 297-317). Academic Press Inc. https://doi.org/10.1016/B978-0-12-385116-1.00017-0
DS Docta Complutense
RD 18 mar 2026