Journal article

Variola virus F1L is a Bcl-2-like protein that unlike its vaccinia virus counterpart inhibits apoptosis independent of Bim

B Marshall, H Puthalakath, S Caria, S Chugh, M Doerflinger, PM Colman, M Kvansakul

Cell Death and Disease | NATURE PUBLISHING GROUP | Published : 2015

Abstract

Subversion of host cell apoptosis is an important survival strategy for viruses to ensure their own proliferation and survival. Certain viruses express proteins homologous in sequence, structure and function to mammalian pro-survival B-cell lymphoma 2 (Bcl-2) proteins, which prevent rapid clearance of infected host cells. In vaccinia virus (VV), the virulence factor F1L was shown to be a potent inhibitor of apoptosis that functions primarily be engaging pro-apoptotic Bim. Variola virus (VAR), the causative agent of smallpox, harbors a homolog of F1L of unknown function. We show that VAR F1L is a potent inhibitor of apoptosis, and unlike all other characterized anti-apoptotic Bcl-2 family mem..

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University of Melbourne Researchers

Grants

Awarded by National Science Foundation


Funding Acknowledgements

We thank A Wardak for technical assistance; staff at the Australian Synchrotron for assistance with diffraction data collection; CSIRO C3 Centre for assistance with crystallization. This work was supported by the National Health and Medical Research Council Australia (Project Grant APP1007918 and Fellowship 637372 to MK, Fellowship and Program Grant to PMC), Australian Research Council (Fellowship FT130101349 to MK), the Cooperative Research Center for Biomarker Translation (scholarship to BM), the Victorian State Government Operational Infrastructure Support and the Australian Government NHMRC IRIISS. Data deposition: Coordinates for F1L were deposited with the Protein Data Bank, accession code 5ajj and 5ajk.