about
Exploring the HIFs, buts and maybes of hypoxia signalling in disease: lessons from zebrafish modelsHypoxia inducible factor signaling modulates susceptibility to mycobacterial infection via a nitric oxide dependent mechanismSuccinate is an inflammatory signal that induces IL-1β through HIF-1α.Functional redundancy of class I phosphoinositide 3-kinase (PI3K) isoforms in signaling growth factor-mediated human neutrophil survivalA zebrafish compound screen reveals modulation of neutrophil reverse migration as an anti-inflammatory mechanism.Hypoxia selectively inhibits respiratory burst activity and killing of Staphylococcus aureus in human neutrophils.What can we learn from highly purified neutrophils?MET is required for the recruitment of anti-tumoural neutrophilsThe role of HIF-1alpha in myeloid cell inflammation.Deficiency of tumour necrosis factor-related apoptosis-inducing ligand exacerbates lung injury and fibrosis.Hypoxia-induced neutrophil survival is mediated by HIF-1alpha-dependent NF-kappaB activity.Roles of neutrophils in the regulation of the extent of human inflammation through delivery of IL-1 and clearance of chemokinesThe HIF/VHL pathway: from oxygen sensing to innate immunity.Hypoxia-inducible factor 2α regulates key neutrophil functions in humans, mice, and zebrafish.Hypoxia, the HIF pathway and neutrophilic inflammatory responses.The regulation of pulmonary inflammation by the hypoxia-inducible factor-hydroxylase oxygen-sensing pathway.Prolyl hydroxylase 2 inactivation enhances glycogen storage and promotes excessive neutrophilic responses.Prolyl hydroxylase 3 (PHD3) is essential for hypoxic regulation of neutrophilic inflammation in humans and miceMutations in succinate dehydrogenase B (SDHB) enhance neutrophil survival independent of HIF-1α expressionDistinct cell death programs in monocytes regulate innate responses following challenge with common causes of invasive bacterial disease.Involvement of a ferroprotein sensor in hypoxia-mediated inhibition of neutrophil apoptosis.The survival effect of TNF-alpha in human neutrophils is mediated via NF-kappa B-dependent IL-8 release.z-VAD-fmk augmentation of TNF alpha-stimulated neutrophil apoptosis is compound specific and does not involve the generation of reactive oxygen species.Cezanne regulates inflammatory responses to hypoxia in endothelial cells by targeting TRAF6 for deubiquitination.Activation of hypoxia-inducible factor-1α (Hif-1α) delays inflammation resolution by reducing neutrophil apoptosis and reverse migration in a zebrafish inflammation model.Pseudomonas expression of an oxygen sensing prolyl hydroxylase homologue regulates neutrophil host responses in vitro and in vivo.Characterization of the survival effect of tumour necrosis factor-alpha in human neutrophils.A local circadian clock calls time on lung inflammation.Opsonic Phagocytosis in Chronic Obstructive Pulmonary Disease is Enhanced by Nrf2 Agonists.Hypoxia and host pathogen responses.Neutrophils from patients with heterozygous germline mutations in the von Hippel Lindau protein (pVHL) display delayed apoptosis and enhanced bacterial phagocytosisHypoxia and the regulation of myeloid cell metabolic imprinting: consequences for the inflammatory responseInflammation and Hypoxia: HIF and PHD Isoform SelectivityGetting DAMP(s) Wets the Whistle for Neutrophil RecruitmentThe role of neutrophils in cancerNeutrophil energetics and oxygen sensingIL4Rα Signaling Abrogates Hypoxic Neutrophil Survival and Limits Acute Lung Injury Responses In VivoRate of replenishment and microenvironment contribute to the sexually dimorphic phenotype and function of peritoneal macrophages
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description
researcher ORCID ID = 0000-0001-9584-174X
@en
name
Sarah R Walmsley
@ast
Sarah R Walmsley
@en
Sarah R Walmsley
@nl
type
label
Sarah R Walmsley
@ast
Sarah R Walmsley
@en
Sarah R Walmsley
@nl
prefLabel
Sarah R Walmsley
@ast
Sarah R Walmsley
@en
Sarah R Walmsley
@nl
P21
P31
P496
0000-0001-9584-174X