R
Rowena S. Lewis
Researcher at Walter and Eliza Hall Institute of Medical Research
Publications - 22
Citations - 2187
Rowena S. Lewis is an academic researcher from Walter and Eliza Hall Institute of Medical Research. The author has contributed to research in topics: Zebrafish & Nitric oxide synthase. The author has an hindex of 14, co-authored 21 publications receiving 1839 citations. Previous affiliations of Rowena S. Lewis include Deakin University & Centre for Cellular and Molecular Biology.
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Journal ArticleDOI
The Pseudokinase MLKL Mediates Necroptosis via a Molecular Switch Mechanism
James M. Murphy,Peter E. Czabotar,Peter E. Czabotar,Joanne M Hildebrand,Joanne M Hildebrand,Isabelle S Lucet,Jian-Guo Zhang,Jian-Guo Zhang,Silvia Alvarez-Diaz,Silvia Alvarez-Diaz,Rowena S. Lewis,Rowena S. Lewis,Najoua Lalaoui,Najoua Lalaoui,Donald Metcalf,Donald Metcalf,Andrew I. Webb,Andrew I. Webb,Samuel N. Young,Samuel N. Young,Leila N. Varghese,Leila N. Varghese,Gillian M. Tannahill,Gillian M. Tannahill,Esme C. Hatchell,Esme C. Hatchell,Ian J. Majewski,Ian J. Majewski,Toru Okamoto,Toru Okamoto,Renwick C. J. Dobson,Renwick C. J. Dobson,Douglas J. Hilton,Douglas J. Hilton,Jeffrey J. Babon,Jeffrey J. Babon,Nicos A. Nicola,Nicos A. Nicola,Andreas Strasser,Andreas Strasser,John Silke,John Silke,Warren S. Alexander,Warren S. Alexander +43 more
TL;DR: Structural-guided mutation of the MLKL pseudoactive site resulted in constitutive, RIPK3-independent necroptosis, demonstrating that modification ofMLKL is essential for propagation of the ne croptosis pathway downstream of RIPK 3.
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Cytokine receptor signaling through the Jak-Stat-Socs pathway in disease.
TL;DR: This review represents an overview of the current understanding of the cytokine receptors, Janus kinases, Signal transducers and activators of transcription, and Suppressors of cytokine signaling, focussing on their contribution to diseases of an immune or hematologic nature.
Journal ArticleDOI
The Pathogen Candida albicans Hijacks Pyroptosis for Escape from Macrophages
Nathalie Uwamahoro,Jiyoti Verma-Gaur,Hsin-Hui Shen,Yue Qu,Rowena S. Lewis,Rowena S. Lewis,Jingxiong Lu,Keith R. Bambery,Seth L. Masters,Seth L. Masters,James E Vince,James E Vince,Thomas Naderer,Ana Traven +13 more
TL;DR: The data provide a new model for how the interplay between fungal morphogenesis and activation of a host cell death pathway mediates macrophage killing by C. albicans hyphae and suggest that the defects of the Mediator mutants in causing macrophages death are caused, at least in part, by reduced activation of pyroptosis.
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
The SPRY domain-containing SOCS box protein SPSB2 targets iNOS for proteasomal degradation.
Zhihe Kuang,Rowena S. Lewis,Joan M Curtis,Yifan Zhan,Bernadette M. Saunders,Jeffrey J. Babon,Tatiana B. Kolesnik,Andrew Low,Seth L. Masters,Tracy A. Willson,Lukasz Kedzierski,Shenggen Yao,Emanuela Handman,Raymond S. Norton,Sandra E. Nicholson +14 more
TL;DR: Macrophages lacking SPSB2 have increased NO production and enhanced pathogen-killing capabilities due to decreased ubiquitin-mediated destruction of iNOS.