Fig. 6: Bcl-xL reduces Ca2+-dependent ER stress by closing the IP3R channel. | Cell Death Discovery

Fig. 6: Bcl-xL reduces Ca2+-dependent ER stress by closing the IP3R channel.

From: The endoplasmic reticulum pool of Bcl-xL prevents cell death through IP3R-dependent calcium release

Fig. 6

Proposed model for the role of Bcl-xL at the ER. Left panel: ER stress might induce ER Ca2+ release in the cytosol (yellow dots), promoting Ca2+ uptake by the mitochondria and subsequent apoptosis initiation through mPTP opening and cytochrome C release in the cytosol (red diamonds). Right panel: ER-targeted Bcl-xL interacts with IP3R and closes the channel, abrogating ER Ca2+ depletion and downstream apoptosis. This model highlights a new indirect anti-apoptotic function of Bcl-xL upon ER stress.

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