Inhibiting Bcl-2 via its BH4 domain in DLBCL cancers to provoke pro-apoptotic Ca2+ signaling

Authors

  • Martijn Kerkhofs KU Leuven

Abstract

Some DLBCL cancers are sensitized to programmed cell death at the ER by upregulation of the IP3R2. These cancers express Bcl-2 in abundance to prevent pro-apoptotic IP3R2-mediated Ca2+ signaling. BIRD-2 (Bcl-2/IP3R Disruptor-2) is a newly developed peptide that disrupts the complex of Bcl-2 and the IP3R, thereby provoking toxic Ca2+ signaling. However, the exact working mechanism of this peptide has not been characterized. We report a possible role for the mitochondria as downstream effectors of BIRD-2-induced cell death and validated a calcein-AM/CoCl2 staining to assess mPTP opening in response to BIRD-2.

Author Biography

Martijn Kerkhofs, KU Leuven

Laboratory of Molecular and Cellular Signaling, Department of Cellular and Molecular Medicine,

References

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Published

2015-11-20

How to Cite

Kerkhofs, M. (2015). Inhibiting Bcl-2 via its BH4 domain in DLBCL cancers to provoke pro-apoptotic Ca2+ signaling. Student Undergraduate Research E-Journal!, 1. Retrieved from https://journals.open.tudelft.nl/sure/article/view/1071

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Section

Economics & Social Sciences