M
Michael J. White
Researcher at University of Melbourne
Publications - 14
Citations - 1781
Michael J. White is an academic researcher from University of Melbourne. The author has contributed to research in topics: Platelet & Apoptosis. The author has an hindex of 11, co-authored 14 publications receiving 1437 citations. Previous affiliations of Michael J. White include Walter and Eliza Hall Institute of Medical Research.
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Journal ArticleDOI
Apoptotic Caspases Suppress mtDNA-Induced STING-Mediated Type I IFN Production
Michael J. White,Michael J. White,Kate McArthur,Kate McArthur,Donald Metcalf,Donald Metcalf,Rachael M. Lane,John C. Cambier,Marco J Herold,Marco J Herold,Mark F. van Delft,Mark F. van Delft,Sammy Bedoui,Guillaume Lessene,Guillaume Lessene,Matthew E. Ritchie,Matthew E. Ritchie,David C.S. Huang,David C.S. Huang,Benjamin T. Kile,Benjamin T. Kile +20 more
TL;DR: The apoptotic caspase cascade functions to render mitochondrial apoptosis immunologically silent, and suppresses type I interferon (IFN) production by cells undergoing Bak/Bax-mediated apoptosis.
Journal ArticleDOI
Two distinct pathways regulate platelet phosphatidylserine exposure and procoagulant function
Simone M. Schoenwaelder,Yuping Yuan,Emma C. Josefsson,Michael J. White,Yu Yao,Kylie D. Mason,Lorraine A. O'Reilly,Katya J. Henley,Akiko Ono,Sarah Tzu-Feng Hsiao,Abbey Willcox,Andrew W. Roberts,David C.S. Huang,Hatem H. Salem,Benjamin T. Kile,Shaun P. Jackson +15 more
TL;DR: 2 distinct pathways regulating the procoagulant function of platelets are shown, one of which is Bak/Bax- and caspase-dependent and the other is agonist-induced, which was completely eliminated by extracellular calcium chelators or inhibitors of platelet activation.
Journal ArticleDOI
Bcl-xL inhibitory BH3 mimetics can induce a transient thrombocytopathy that undermines the hemostatic function of platelets
Simone M. Schoenwaelder,Kate E. Jarman,Elizabeth E. Gardiner,My Hua,Jianlin Qiao,Michael J. White,Michael J. White,Emma C. Josefsson,Imala Alwis,Akiko Ono,Abbey Willcox,Robert K. Andrews,Kylie D. Mason,Hatem H. Salem,David C.S. Huang,David C.S. Huang,Benjamin T. Kile,Benjamin T. Kile,Andrew W. Roberts,Andrew W. Roberts,Shaun P. Jackson +20 more
TL;DR: These studies demonstrate that Bcl-x(L)-inhibitory BH3 mimetics not only induce thrombocytopenia but also a transient thromBocytopathy that can undermine the hemostatic function of platelets.
Journal ArticleDOI
Mitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome priming
Ramanjaneyulu Allam,Kate E. Lawlor,Kate E. Lawlor,Eric Chi-Wang Yu,Alison L Mildenhall,Alison L Mildenhall,Donia M Moujalled,Donia M Moujalled,Rowena S. Lewis,Rowena S. Lewis,Francine Ke,Francine Ke,Kylie D. Mason,Kylie D. Mason,Michael J. White,Michael J. White,Katryn J. Stacey,Andreas Strasser,Andreas Strasser,Lorraine A. O'Reilly,Lorraine A. O'Reilly,Warren S. Alexander,Warren S. Alexander,Benjamin T. Kile,Benjamin T. Kile,David L. Vaux,David L. Vaux,James E Vince,James E Vince +28 more
TL;DR: It is demonstrated that mitochondrial apoptosis is not required for NLRP3 activation, and an important non‐apoptotic role for caspase‐8 is highlighted in regulating inflammasome activation and pro‐inflammatory cytokine levels.
Journal ArticleDOI
Megakaryocytes possess a functional intrinsic apoptosis pathway that must be restrained to survive and produce platelets
Emma C. Josefsson,Chloé James,Katya J. Henley,Marlyse A. Debrincat,Marlyse A. Debrincat,Kelly L. Rogers,Kelly L. Rogers,Mark R. Dowling,Mark R. Dowling,Michael J. White,Michael J. White,Elizabeth A. Kruse,Elizabeth A. Kruse,Rachael M. Lane,Sarah Ellis,Paquita Nurden,Kylie D. Mason,Kylie D. Mason,Lorraine A. O'Reilly,Lorraine A. O'Reilly,Andrew W. Roberts,Andrew W. Roberts,Donald Metcalf,Donald Metcalf,David C.S. Huang,David C.S. Huang,Benjamin T. Kile,Benjamin T. Kile +27 more
TL;DR: Deletion of Bak and Bax, the effectors of mitochondrial apoptosis, does not affect platelet production, however, loss of prosurvival Bcl-xL results in megakaryocyte apoptosis and failure of platelet shedding.