Search

Your search keyword '"Hampton, Mark B."' showing total 244 results
Start Over Author "Hampton, Mark B." Search Limiters Available in Library Collection
244 results on '"Hampton, Mark B."'

2. Neutrophil-vascular interactions drive myeloperoxidase accumulation in the brain in Alzheimer’s disease

Author

Smyth, Leon C. D., Murray, Helen C., Hill, Madison, van Leeuwen, Eve, Highet, Blake, Magon, Nicholas J., Osanlouy, Mahyar, Mathiesen, Sophie N., Mockett, Bruce, Singh-Bains, Malvindar K., Morris, Vanessa K., Clarkson, Andrew N., Curtis, Maurice A., Abraham, Wickliffe C., Hughes, Stephanie M., Faull, Richard L. M., Kettle, Anthony J., Dragunow, Mike, and Hampton, Mark B.

Published
2022
Full Text
View/download PDF

12. Additional file 1 of Neutrophil-vascular interactions drive myeloperoxidase accumulation in the brain in Alzheimer���s disease

Author

Smyth, Leon C. D., Murray, Helen C., Hill, Madison, van Leeuwen, Eve, Highet, Blake, Magon, Nicholas J., Osanlouy, Mahyar, Mathiesen, Sophie N., Mockett, Bruce, Singh-Bains, Malvindar K., Morris, Vanessa K., Clarkson, Andrew N., Curtis, Maurice A., Abraham, Wickliffe C., Hughes, Stephanie M., Faull, Richard L. M., Kettle, Anthony J., Dragunow, Mike, and Hampton, Mark B.

Abstract

Additional file 1. Figure S1: MPO labelling is predominantly confined to neutrophils. Figure S2: Neutrophil accumulation is independent of sex, age, and post-mortem delay. Figure S3: Regional analysis of neutrophil accumulation in APP/PS1 mice. Figure S4: Amyloid-��1-42 does not induce NETosis in vitro. Figure S5: Specificity of antibody labelling across multiple rounds of multiplexed immunohistochemistry. Table S1: Case details of tissue used in tissue microarray and immunohistochemistry experiments. Table S2: Details of antibodies used for these studies.

Published
2022
Full Text
View/download PDF

17. Additional file 1 of Genome-wide impact of hydrogen peroxide on maintenance DNA methylation in replicating cells

Author

Seddon, Annika R., Yusmiati Liau, Pace, Paul E., Miller, Allison L., Das, Andrew B., Kennedy, Martin A., Hampton, Mark B., and Stevens, Aaron J.

Subjects
ComputingMethodologies_DOCUMENTANDTEXTPROCESSING, ComputingMilieux_COMPUTERSANDEDUCATION, Data_FILES, ComputerApplications_COMPUTERSINOTHERSYSTEMS
Abstract

Additional file 1. Supplementary tables and figures.

Published
2021
Full Text
View/download PDF

21. Oxidation of bacillithiol during killing of Staphylococcus aureusUSA300 inside neutrophil phagosomes

Author

Ashby, Louisa V, Springer, Reuben, Loi, Vu Van, Antelmann, Haike, Hampton, Mark B, Kettle, Anthony J, and Dickerhof, Nina

Abstract

Targeting immune evasion tactics of pathogenic bacteria may hold the key to treating recalcitrant bacterial infections. Staphylococcus aureusproduces bacillithiol (BSH), its major low‐molecular‐weight thiol, which is thought to protect this opportunistic human pathogen against the bombardment of oxidants inside neutrophil phagosomes. Here, we show that BSH was oxidized when human neutrophils phagocytosed S. aureus, but provided limited protection to the bacteria. We used mass spectrometry to measure the oxidation of BSH upon exposure of S. aureusUSA300 to either a bolus of hypochlorous acid (HOCl) or a flux generated by the neutrophil enzyme myeloperoxidase. Oxidation of BSH and loss of bacterial viability were strongly correlated (r= 0.99, p< 0.001). BSH was fully oxidized after exposure of S. aureusto lethal doses of HOCl. However, there was no relationship between the initial BSH levels and the dose of HOCl required for bacterial killing. In contrast to the HOCl systems, only 50% of total BSH was oxidized when neutrophils killed the majority of phagocytosed bacteria. Oxidation of BSH was decreased upon inhibition of myeloperoxidase, implicating HOCl in phagosomal BSH oxidation. A BSH‐deficient S. aureusUSA300 mutant was slightly more susceptible to treatment with either HOCl or ammonia chloramine, or to killing within neutrophil phagosomes. Collectively, our data show that myeloperoxidase‐derived oxidants react with S. aureusinside neutrophil phagosomes, leading to partial BSH oxidation, and contribute to bacterial killing. However, BSH offers only limited protection against the neutrophil's multifaceted killing mechanisms. Bacterial bacillithiol was oxidized during phagocytosis but provided minimal protection against the neutrophil's killing mechanisms.

Published
2022
Full Text
View/download PDF

27. Hairpin-bisulfite sequencing of cells exposed to decitabine documents the process of DNA demethylation.

Author

Mayyas, Issam M, Weeks, Robert J, Day, Robert C, Magrath, Helena E, O'Connor, Karina M, Kardailsky, Olga, Hore, Timothy A, Hampton, Mark B, and Morison, Ian M

Subjects
DNA demethylation, COMPLEMENTARY DNA, DECITABINE, DNA methylation, METHYLATION, DNA methyltransferases
Abstract

Although the mechanism of DNA demethylating drugs has been understood for many years, the direct effect of these drugs on methylation of the complementary strands of DNA has not been formally demonstrated. By using hairpin-bisulphite sequencing, we describe the kinetics and pattern of DNA methylation following treatment of cells by the DNA methyltransferase 1 (DNMT1) inhibitor, decitabine. As expected, we demonstrate complete loss of methylation on the daughter strand following S-phase in selected densely methylated genes in synchronized Jurkat cells. Thereafter, cells showed a heterogeneous pattern of methylation reflecting replication of the unmethylated strand and restoration of methylation. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

31. Induction of the reactive chlorine-responsive transcription factor RclR in Escherichia coli following ingestion by neutrophils.

Author

Königstorfer, Andreas, Ashby, Louisa V, Bollar, Gretchen E, Billiot, Caitlin E, Gray, Michael J, Jakob, Ursula, Hampton, Mark B, and Winterbourn, Christine C

Subjects
TRANSCRIPTION factors, ESCHERICHIA coli, NEUTROPHILS, INGESTION, HYPOCHLORITES, PHAGOCYTOSIS
Abstract

Neutrophils generate hypochlorous acid (HOCl) and related reactive chlorine species as part of their defence against invading microorganisms. In isolation, bacteria respond to reactive chlorine species by upregulating responses that provide defence against oxidative challenge. Key questions are whether these responses are induced when bacteria are phagocytosed by neutrophils, and whether this provides them with a survival advantage. We investigated RclR, a transcriptional activator of the rclABC operon in Escherichia coli that has been shown to be specifically activated by reactive chlorine species. We first measured induction by individual reactive chlorine species, and showed that HOCl itself activates the response, as do chloramines (products of HOCl reacting with amines) provided they are cell permeable. Strong RclR activation was seen in E. coli following phagocytosis by neutrophils, beginning within 5 min and persisting for 40 min. RclR activation was suppressed by inhibitors of NOX2 and myeloperoxidase, providing strong evidence that it was due to HOCl production in the phagosome. RclR activation demonstrates that HOCl, or a derived chloramine, enters phagocytosed bacteria in sufficient amount to induce this response. Although RclR was induced in wild-type bacteria following phagocytosis, we detected no greater sensitivity to neutrophil killing of mutants lacking genes in the rclABC operon. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

35. Introduction to special issue on mitochondrial redox signaling in health and disease

Author

Biotechnology and Biological Sciences Research Council (UK), Parkinson's Disease Society (UK), British Heart Foundation, National Institutes of Health (US), Bolaños, Juan P., Cadenas, Enrique, Duchen, Michael R., Hampton, Mark B., Mann, Giovanni E., Murphy, Michael P., Biotechnology and Biological Sciences Research Council (UK), Parkinson's Disease Society (UK), British Heart Foundation, National Institutes of Health (US), Bolaños, Juan P., Cadenas, Enrique, Duchen, Michael R., Hampton, Mark B., Mann, Giovanni E., and Murphy, Michael P.

Abstract

Mitochondria are functional entities that harbor the energy-conservation machinery that supports cell function through the coordination of mitochondrion-derived molecules involved in the regulation of cell signaling and transcription. Conversely, mitochondria are targets of an ever-increasing number of signaling pathways and their activity is also modulated by several transcription factors. The cell's energy-redox homeostasis is primarily a function of mitochondrial oxidative phosphorylation and the formation of O2.–/H2O2. Notably, other mitochondrion-driven processes contribute to cellular homeostasis, such as mitochondrial biogenesis and dynamics, mitochondrial quality control (autophagy and mitophagy), mitochondrial proteostasis and the role of the mitochondrial unfolded protein response (UPRmt), and redox signaling in the homeostatic control of mitochondrial function. This Free Radical Biology & Medicine special issue on Mitochondrial Redox Signaling in Health and Disease covers some aspects of the myriad of processes embraced by mitochondrial biology and physiology, provides mechanistic insights linking mitochondrial function with cell function, and recognizes mitochondrial function as an amenable therapeutic target.

Published
2016

44. Hyperoxidation of Peroxiredoxins 2 and 3

Author

Peskin, Alexander V., primary, Dickerhof, Nina, additional, Poynton, Rebecca A., additional, Paton, Louise N., additional, Pace, Paul E., additional, Hampton, Mark B., additional, and Winterbourn, Christine C., additional

Published
2013
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results