K
Kate E. Lawlor
Researcher at Hudson Institute of Medical Research
Publications - 69
Citations - 6520
Kate E. Lawlor is an academic researcher from Hudson Institute of Medical Research. The author has contributed to research in topics: Inflammasome & Programmed cell death. The author has an hindex of 32, co-authored 59 publications receiving 5157 citations. Previous affiliations of Kate E. Lawlor include Royal Children's Hospital & Walter and Eliza Hall Institute of Medical Research.
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Journal ArticleDOI
ADAMTS5 is the major aggrecanase in mouse cartilage in vivo and in vitro
Heather Stanton,Fraser M. Rogerson,Charlotte J. East,Suzanne B. Golub,Kate E. Lawlor,Clare T. Meeker,Christopher B. Little,Pamela J. Farmer,Ian K. Campbell,Fourie Anne M,Amanda J. Fosang +10 more
TL;DR: The data suggest that ADAMts5 may be a suitable target for the development of new drugs designed to inhibit cartilage destruction in arthritis, although further work will be required to determine whether ADAMTS5 is also the major aggrecanase in human arthritis.
Journal ArticleDOI
RIPK1 regulates RIPK3-MLKL-driven systemic inflammation and emergency hematopoiesis.
James A Rickard,James A Rickard,Joanne A. O’Donnell,Joanne A. O’Donnell,Joseph M Evans,Joseph M Evans,Najoua Lalaoui,Najoua Lalaoui,Ashleigh R Poh,Ashleigh R Poh,TeWhiti Rogers,James E Vince,James E Vince,Kate E. Lawlor,Kate E. Lawlor,Robert L Ninnis,Robert L Ninnis,Holly Anderton,Holly Anderton,Cathrine Hall,Cathrine Hall,Sukhdeep K Spall,Sukhdeep K Spall,Toby J. Phesse,Toby J. Phesse,Helen E. Abud,Louise H. Cengia,Louise H. Cengia,Jason Corbin,Jason Corbin,Sandra Mifsud,Sandra Mifsud,Ladina Di Rago,Ladina Di Rago,Donald Metcalf,Donald Metcalf,Matthias Ernst,Matthias Ernst,Grant Dewson,Grant Dewson,Andrew W. Roberts,Andrew W. Roberts,Warren S. Alexander,Warren S. Alexander,James M. Murphy,James M. Murphy,Paul G Ekert,Paul G Ekert,Seth L. Masters,Seth L. Masters,David L. Vaux,David L. Vaux,Ben A. Croker,Ben A. Croker,Ben A. Croker,Motti Gerlic,Motti Gerlic,Motti Gerlic,John Silke,John Silke +59 more
TL;DR: A key function for RIPK1 is revealed in inhibiting necroptosis and, thereby, a role in limiting, not only promoting, inflammation is revealed.
Journal ArticleDOI
RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL
Kate E. Lawlor,Nufail Khan,Alison L Mildenhall,Motti Gerlic,Ben A. Croker,Akshay A. D’Cruz,Cathrine Hall,Sukhdeep Kaur. Spall,Holly Anderton,Seth L. Masters,Maryam Rashidi,Ian P. Wicks,Warren S. Alexander,Yasuhiro Mitsuuchi,Christopher A. Benetatos,Stephen M. Condon,W. Wei-Lynn Wong,John Silke,David L. Vaux,James E Vince +19 more
TL;DR: It is shown that following LPS treatment, or LPS-induced necroptosis, the TLR adaptor protein TRIF and inhibitor of apoptosis proteins (IAPs: X-linked IAP, cellular IAP1 and IAP2) regulate RIPK3 and MLKL ubiquitylation, and RIPK 3 can promote NLRP3 inflammasome and IL-1β inflammatory responses independent ofMLKL and necroPTotic cell death.
Journal ArticleDOI
Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation.
James E Vince,W. Wei-Lynn Wong,W. Wei-Lynn Wong,Ian E Gentle,Kate E. Lawlor,Kate E. Lawlor,Ramanjaneyulu Allam,Lorraine A. O'Reilly,Lorraine A. O'Reilly,Kylie D. Mason,Kylie D. Mason,Olaf Gross,Stephen B. Ma,Stephen B. Ma,Greta Guarda,Holly Anderton,Holly Anderton,Rosa Castillo,Georg Häcker,John Silke,John Silke,Jürg Tschopp +21 more
TL;DR: It is demonstrated that activation of the cell death-inducing ripoptosome platform and RIP3 can generate bioactive IL-1β and implicate them as additional targets for the treatment of pathological IL- 1-driven inflammatory responses.
Journal ArticleDOI
Active MLKL triggers the NLRP3 inflammasome in a cell-intrinsic manner.
Stephanie A. Conos,Stephanie A. Conos,Kaiwen W. Chen,Dominic De Nardo,Dominic De Nardo,Hideki Hara,Lachlan Whitehead,Lachlan Whitehead,Gabriel Núñez,Seth L. Masters,Seth L. Masters,James M. Murphy,James M. Murphy,Kate Schroder,David L. Vaux,David L. Vaux,Kate E. Lawlor,Kate E. Lawlor,Lisa M Lindqvist,Lisa M Lindqvist,James E Vince,James E Vince +21 more
TL;DR: It is shown that MLKL-mediated NLRP3 and caspase-1 activation and the secretion of the proinflammatory cytokine IL-1β is a major determinant of necroptotic-derived inflammatory signals, and the findings suggest that NL RP3 and IL- 1β may be relevant therapeutic targets in MLK lysis-driven diseases.