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

  • 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.

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Author Biography

Martijn Kerkhofs, KU Leuven
Laboratory of Molecular and Cellular Signaling, Department of Cellular and Molecular Medicine,
How to Cite
KERKHOFS, Martijn. Inhibiting Bcl-2 via its BH4 domain in DLBCL cancers to provoke pro-apoptotic Ca2+ signaling. Student Undergraduate Research E-journal!, [S.l.], v. 1, nov. 2015. ISSN 2468-0443. Available at: <https://journals.open.tudelft.nl/index.php/sure/article/view/1071>. Date accessed: 25 mar. 2019.
Published
2015-11-20