scispace - formally typeset
K

Katryn J. Stacey

Researcher at University of Queensland

Publications -  99
Citations -  8443

Katryn J. Stacey is an academic researcher from University of Queensland. The author has contributed to research in topics: Inflammasome & CpG site. The author has an hindex of 46, co-authored 95 publications receiving 7346 citations. Previous affiliations of Katryn J. Stacey include University of Cambridge & Duke University.

Papers
More filters
Journal ArticleDOI

HIN-200 proteins regulate caspase activation in response to foreign cytoplasmic DNA.

TL;DR: This work identifies the HIN-200 family member and candidate lupus susceptibility factor, p202, as a dsDNA binding protein that bound stably and rapidly to transfected DNA and indicates that Hin-200 proteins can act as pattern recognition receptors mediating responses to cytoplasmic ds DNA.
Journal Article

Macrophages ingest and are activated by bacterial DNA.

TL;DR: Results suggest that DNA is taken up by macrophages and characteristic bacterial DNA sequences, which include an unmethylated CpG sequence, activate a signaling cascade leading to activation of NF-kappa B and inflammatory gene induction.
Journal ArticleDOI

Dengue virus NS1 protein activates cells via Toll-like receptor 4 and disrupts endothelial cell monolayer integrity

TL;DR: It is shown that the secreted form of the dengue virus nonstructural protein 1 (NS1) is a pathogen-associated molecular pattern (PAMP) that activates mouse macrophages and human peripheral blood mononuclear cells (PBMCs) in culture via Toll-like receptor 4 (TLR4), resulting in release of inflammatory cytokines—an effect that was blocked by either a TLR4 antagonist or an anti-TLR 4 antibody.
Journal ArticleDOI

Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity

TL;DR: It is reported that in the cell, the dominant species of active caspase-1 dimers elicited by inflammasomes are in fact full-length p46 and a transient species, p33/p10, which offers a molecular basis for the transient nature, and coordinated timing, ofinflammasome-dependent inflammatory responses.