Journal article
Pro-apoptotic BIM is an essential initiator of physiological endothelial cell death independent of regulation by FOXO3
MN Koenig, E Naik, L Rohrbeck, MJ Herold, E Trounson, P Bouillet, T Thomas, AK Voss, A Strasser, L Coultas
CELL DEATH AND DIFFERENTIATION | NATURE PUBLISHING GROUP | Published : 2014
DOI: 10.1038/cdd.2014.90
Abstract
The growth of new blood vessels by angiogenesis is essential for normal development, but can also cause or contribute to the pathology of numerous diseases. Recent studies have shown that BIM, a pro-apoptotic BCL2-family protein, is required for endothelial cell apoptosis in vivo, and can contribute to the anti-angiogenic effect of VEGF-A inhibitors in certain tumor models. Despite its importance, the extent to which BIM is autonomously required for physiological endothelial apoptosis remains unknown and its regulation under such conditions is poorly defined. While the transcription factor FOXO3 has been proposed to induce Bim in response to growth factor withdrawal, evidence for this functi..
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Awarded by National Health and Medical Research Council, Australia
Awarded by Leukemia & Lymphoma Society (Special Center of Research)
Awarded by Australian Research Council Future Fellowship
Funding Acknowledgements
We thank Lachlan Whitehead, Cameron Nowell and Kelly Rogers for expert imaging assistance, Lisa Sampurno for technical assistance, Merle Dayton, Keti Stoev, Chrystal Smith and Emma Lanera for expert animal care and members of the Development and Cancer Division (WEHI) for informative discussion. This work was made possible through Victorian State Government Operational Infrastructure Support and Australian Government NHMRC IRIISS. This work was supported by the National Health and Medical Research Council, Australia (project grants: 1010638,1046010 and 1049720, program grants: 1016701, and fellowships to TT (1003435), AKV (575512) and AS (1020363)) and Leukemia & Lymphoma Society (Special Center of Research 7001-13). LC is supported by an Australian Research Council Future Fellowship (110100891).