ARAN - Access to Research at NUI Galway

Bcl-2 family on guard at the ER

ARAN - Access to Research at NUI Galway

Show simple item record Samali, Afshin en Sanjeev, Gupta en Ní Chonghaile, Tríona en MacDonald, David C en Szegezdi, Eva en 2009-04-30T09:10:24Z en 2009-04-30T09:10:24Z en 2009 en
dc.identifier.uri en
dc.description.abstract The endoplasmic reticulum (ER) is the main site for protein folding, lipid biosynthesis and calcium storage in the cell. Disturbances of these critical cellular functions lead to ER stress. The ER responds to disturbances in its homeostasis by launching an adaptive signal transduction pathway, known as the unfolded protein response (UPR). The UPR strives to maintain ER function during stress; however, if the stress is not resolved apoptotic responses are activated that involve crosstalk between the ER and mitochondria. In addition, ER stress is also known to induce autophagy to counteract XBP-1 mediated ER expansion and assist in the degradation of unfolded proteins. One family of proteins involved in the regulation of apoptosis is that of Bcl-2. Complex interactions among the three subgroups within the Bcl-2 family (the anti- apoptotic, the multi-domain pro-apoptotic and the BH3-only members) control the signaling events of apoptosis upstream of mitochondrial outer membrane permeabilization. These proteins were found have diverse subcellular locations to aid in the response to varied intrinsic and extrinsic stimuli. Of recent interest is the presence of the Bcl-2 family at the ER. Here, we review the involvement of proteins from each of the three Bcl-2 family subgroups in the maintenance of ER homeostasis and their participation in ER stress signaling transduction pathways. en
dc.format application/pdf en
dc.language.iso en en
dc.publisher American Physiological Society en
dc.subject Apoptosis en
dc.subject Ire1 en
dc.subject Unfolded Protein Response (UPR) en
dc.subject Stress en
dc.subject Endoplasmic reticulum (ER) en
dc.subject Bcl-2 family en
dc.title Bcl-2 family on guard at the ER en
dc.type Article en
dc.identifier.doi doi:10.1152/ajpcell.00612.2008 en
dc.local.publishedsource TBC en

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