CDIP1-BAP31 Complex Transduces Apoptotic Signals from Endoplasmic Reticulum to Mitochondria under Endoplasmic Reticulum Stress

Takushi Namba, Fang Tian, Kiki Chu, So Young Hwang, Kyoung Wan Yoon, Sanguine Byun, Masatsugu Hiraki, Anna Mandinova, Sam W. Lee

Research output: Contribution to journalArticlepeer-review

70 Citations (Scopus)


Resolved endoplasmic reticulum (ER) stress response is essential for intracellular homeostatic balance, but unsettled ER stress can lead to apoptosis. Here, we show that a proapoptotic p53 target, CDIP1, acts as a key signal transducer of ER-stress-mediated apoptosis. We identify B-cell-receptor-associated protein 31 (BAP31) as an interacting partner of CDIP1. Upon ER stress, CDIP1 is induced and enhances an association with BAP31 at the ER membrane. We also show that CDIP1 binding to BAP31 is required for BAP31 cleavage upon ER stress and for BAP31-Bcl-2 association. The recruitment of Bcl-2 to the BAP31-CDIP1 complex, as well as CDIP1-dependent truncated Bid (tBid) and caspase-8 activation, contributes to BAX oligomerization. Genetic knockout of CDIP1 in mice leads to impaired response to ER-stress-mediated apoptosis. Altogether, our data demonstrate that the CDIP1/BAP31-mediated regulation of mitochondrial apoptosis pathway represents a mechanism for establishing an ER-mitochondrial crosstalk for ER-stress-mediated apoptosis signaling

Original languageEnglish
Pages (from-to)331-339
Number of pages9
JournalCell Reports
Issue number2
Publication statusPublished - 2013

Bibliographical note

Funding Information:
LC-MS/MS analysis was performed by the Taplin Biological Mass Spectrometry Facility of Harvard Medical School. We thank S. Aaronson for helpful advice and suggestions during the project. This work was partially supported by National Institutes of Health grants CA142805, CA080058, and CA127247. T.N. was supported by a fellowship for research abroad from Japan Society for the Promotion of Science and is a recipient of an AACR-Bristol-Myers Squibb Oncology Scholar-in-Training grant. S.-Y.H. was supported by the Korean Government Research Foundation (KRF-2008-357-E00023).

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)


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