2026 Kate E. Lawlor: Biology and Biochemistry Researcher – H-Index, Publications & Awards

Discipline name	D-Index	World Ranking	Current World Ranking	National Ranking	Current National Ranking	Publications	Citations
Biology and Biochemistry	40	19578	17937	590	566	69	9056

Overview

Kate E. Lawlor is affiliated with the Hudson Institute of Medical Research in Australia. Their research primarily intersects the fields of immunology, microbiology, biochemistry, genetics, molecular biology, and medicine. Through these disciplines, Lawlor has contributed to understanding complex biological and immune processes.

The main fields of study encompass:

Immunology and Microbiology
Biochemistry, Genetics and Molecular Biology
Medicine

Their work narrows down to several subfields, including:

Immunology
Molecular Biology
Infectious Diseases
Epidemiology
Hematology

Kate E. Lawlor has researched extensively on topics such as:

Inflammasome and immune disorders
Interferon and immune responses
Cell death mechanisms and regulation
Immune Response and Inflammation
Immune Cell Function and Interaction
Phagocytosis and Immune Regulation
Autoimmune and Inflammatory Disorders Research

Their frequent publication venues include:

bioRxiv (Cold Spring Harbor Laboratory)
Cell Death and Disease
Cell Reports
Immunity
Nature Communications

Recent papers authored or coauthored by Kate E. Lawlor include:

TBK1 and IKKε Act Redundantly to Mediate STING-Induced NF-κB Responses in Myeloid Cells, 2020, Cell Reports
Mitochondrial dysfunction caused by outer membrane vesicles from Gram-negative bacteria activates intrinsic apoptosis and inflammation, 2020, Nature Microbiology
Interferon-γ primes macrophages for pathogen ligand-induced killing via a caspase-8 and mitochondrial cell death pathway, 2022, Immunity
The ubiquitylation of IL-1β limits its cleavage by caspase-1 and targets it for proteasomal degradation, 2021, Nature Communications
Die Another Way: Interplay between Influenza A Virus, Inflammation and Cell Death, 2020, Viruses

Kate E. Lawlor frequently collaborates with a group of scientists in related fields, including:

James E. Vince
James M. Murphy
Mary Speir
Daniel S. Simpson
Maryam Rashidi

Best Publications

ADAMTS5 is the major aggrecanase in mouse cartilage in vivo and in vitro

Heather Stanton;Fraser M. Rogerson;Charlotte J. East;Suzanne B. Golub

1004
Citations
RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL

Kate E. Lawlor;Nufail Khan;Alison Mildenhall;Motti Gerlic

660
Citations
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

634
Citations
Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation.

James E. Vince;W. Wei Lynn Wong;W. Wei Lynn Wong;Ian Gentle;Kate E. Lawlor;Kate E. Lawlor

561
Citations
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

474
Citations
TBK1 and IKKε Act Redundantly to Mediate STING-Induced NF-κB Responses in Myeloid Cells.

Katherine R. Balka;Katherine R. Balka;Katherine R. Balka;Cynthia Louis;Cynthia Louis;Tahnee L. Saunders;Amber M. Smith

424
Citations
FcgammaRIIb controls bone marrow plasma cell persistence and apoptosis.

Zou Xiang;Antony J Cutler;Antony J Cutler;Rebecca J Brownlie;Kirsten Fairfax

351
Citations
Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease

Najoua Lalaoui;Najoua Lalaoui;Steven E. Boyden;Hirotsugu Oda;Geryl M. Wood

309
Citations
TNFR1-dependent cell death drives inflammation in Sharpin-deficient mice

James A Rickard;Holly Anderton;Nima Etemadi;Ueli Nachbur

263
Citations
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

244
Citations
Blocking aggrecanase cleavage in the aggrecan interglobular domain abrogates cartilage erosion and promotes cartilage repair

Christopher B. Little;Clare T. Meeker;Suzanne B. Golub;Kate E. Lawlor

236
Citations
Distinct cell-specific control of autoimmunity and infection by FcγRIIb

Rebecca J. Brownlie;Kate E. Lawlor;Heather A. Niederer;Antony J. Cutler

200
Citations
The Mitochondrial Apoptotic Effectors BAX/BAK Activate Caspase-3 and -7 to Trigger NLRP3 Inflammasome and Caspase-8 Driven IL-1β Activation

James E. Vince;James E. Vince;Dominic De Nardo;Dominic De Nardo;Wenqing Gao;Angelina J. Vince

186
Citations
cIAPs and XIAP regulate myelopoiesis through cytokine production in an RIPK1- And RIPK3-dependent manner

W. Wei-Lynn Wong;W. Wei-Lynn Wong;W. Wei-Lynn Wong;James E. Vince;James E. Vince;Najoua Lalaoui;Najoua Lalaoui;Kate E. Lawlor;Kate E. Lawlor

182
Citations
Severe inflammatory arthritis and lymphadenopathy in the absence of TNF

Ian K. Campbell;Kristy O’Donnell;Kate E. Lawlor;Ian P. Wicks

174
Citations
TNF can activate RIPK3 and cause programmed necrosis in the absence of RIPK1.

D M Moujalled;W D Cook;T Okamoto;J J Murphy;J J Murphy

168
Citations
IL-18 Production from the NLRP1 Inflammasome Prevents Obesity and Metabolic Syndrome.

Andrew J. Murphy;Andrew J. Murphy;Michael J. Kraakman;Helene L. Kammoun;Dragana Dragoljevic;Dragana Dragoljevic

165
Citations
Mitochondrial dysfunction caused by outer membrane vesicles from Gram-negative bacteria activates intrinsic apoptosis and inflammation

Pankaj Deo;Seong H Chow;Mei-Ling Han;Mary Speir

155
Citations
Suppressor of cytokine signaling-1 regulates acute inflammatory arthritis and T cell activation

Paul J. Egan;Kate E. Lawlor;Warren S. Alexander;Ian P. Wicks

153
Citations
Author response: TNFR1-dependent cell death drives inflammation in Sharpin-deficient mice

James A Rickard;James A Rickard;Holly Anderton;Holly Anderton;Nima Etemadi;Nima Etemadi;Ueli Nachbur;Ueli Nachbur

1
Citations