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. 2017 Oct 6;8:803. doi: 10.1038/s41467-017-00975-w

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — A schematic depicting that Bik fulfills several functions to facilitate cell death. (1) Bik dissociates Bak/Bcl-2 and interacts with DAPk1 to form a complex with Bak that forms multimers and anchors DAPk1 to the ER to increase the contact sites of ER and mitochondria, (2) Bik disrupts the interaction between Bcl-2 and IP₃R to cause calcium release, and (3) ER-associated Bak interacts with DAPk1 to facilitate mitochondrial calcium uptake