This is a page describing data taken during an experiment at the ISIS Neutron and Muon Source. Information about the ISIS Neutron and Muon Source can be found at https://www.isis.stfc.ac.uk.
The Interplay of apoptosis regulating Bcl-2 proteins at mitochondrial membranes
Abstract: Programmed cell death (apoptosis) is essential for human life. Its intrinsic (mitochondrial) pathway is tightly regulated by pro- and anti-apoptotic members of the Bcl-2 protein family which meet at the mitochondrial outer membrane (MOM) to control its integrity. Upon activation apoptotic proteins such as Bax perforate the MOM causing cell death. To prevent this mechanism in healthy cells anti-apoptotic proteins such as the Bcl-2 membrane protein itself reside in the MOM and inhibit Bax there. Any imbalance can cause disorder like cancer, where often overexpression of the life-guarding Bcl-2 protein ensures their survival and treatment resistance. Here, we aim to use neutron reflectometry to provide a detailed molecular and kinetic insight into the functioning of Bcl-2 by recognising and sequestering Bax at the membrane, a process to keep healthy cells and remove dysfunctional ones.
Principal Investigator: Professor Gerhard Groebner
Local Contact: Dr Luke Clifton
Experimenter: Dr Hanna Wacklin-Knecht
Experimenter: Dr Jörgen Ĺdén
Experimenter: Dr Tamás Milán Nagy
Experimenter: Dr Sophie Ayscough
DOI: 10.5286/ISIS.E.RB2220333
ISIS Experiment Number: RB2220333
Part DOI | Instrument | Public release date | Download Link |
---|---|---|---|
10.5286/ISIS.E.RB2220333-1 | OFFSPEC | 15 March 2026 | Download |
Publisher: STFC ISIS Neutron and Muon Source
Data format: RAW/Nexus
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Data Citation
The recommended format for citing this dataset in a research
publication is as:
[author], [date], [title], [publisher],
[doi]
For Example:
Professor Gerhard Groebner et al; (2023): The Interplay of apoptosis regulating Bcl-2 proteins at mitochondrial membranes, STFC ISIS Neutron and Muon Source, https://doi.org/10.5286/ISIS.E.RB2220333
Data is released under the CC-BY-4.0 license.