PMID:14561754

Citation	Rao, RV, Poksay, KS, Castro-Obregon, S, Schilling, B, Row, RH, del Rio, G, Gibson, BW, Ellerby, HM and Bredesen, DE (2004) Molecular components of a cell death pathway activated by endoplasmic reticulum stress. J. Biol. Chem. 279:177-87
Abstract	Alterations in Ca2+ homeostasis and accumulation of misfolded proteins in the endoplasmic reticulum (ER) cause ER stress that ultimately leads to programmed cell death. Recent studies have shown that ER stress triggers programmed cell death via an alternative intrinsic pathway of apoptosis that, unlike the intrinsic pathway described previously, is independent of Apaf-1 and cytochrome c. In the present work, we have used a set of complementary approaches, including two-dimensional gel electrophoresis coupled with matrix-assisted laser desorption ionization-time-of-flight mass spectrometry and nano-liquid chromatography-electrospray ionization mass spectrometry with tandem mass spectrometry, RNA interference, co-immunoprecipitation, immunodepletion of candidate proteins, and reconstitution studies, to identify mediators of the ER stress-induced cell death pathway. Our data identify two molecules, valosin-containing protein and apoptosis-linked gene-2 (ALG-2), that appear to play a role in mediating ER stress-induced cell death.
Links	PubMed Online version:10.1074/jbc.M304490200
Keywords	Apoptosis/physiology; Cell Death/physiology; Cell Fractionation; Cell Line; Cell-Free System; Endoplasmic Reticulum/drug effects; Endoplasmic Reticulum/physiology; Humans; Luciferases/genetics; Luciferases/metabolism; Microsomes/physiology; RNA, Small Interfering/genetics; Recombinant Proteins/metabolism; Spectrometry, Mass, Electrospray Ionization; Stress, Mechanical; Thapsigargin/pharmacology
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.