John P. Boyle
University of Leeds
76 Papers
376 Citations
John P. Boyle is an academic researcher from University of Leeds. The author has contributed to research in topics: Hypoxia (medical) & Biology. The author has an hindex of 29, co-authored 76 publications.
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Papers
Hypoxia suppresses glutamate transport in astrocytes.
Mark L. Dallas,Hannah E. Boycott,Lucy Atkinson,Alison Miller,John P. Boyle,Hugh A. Pearson,Chris Peers +6 more
TL;DR: The results indicate that prolonged hypoxia can suppress glutamate uptake in astrocytes and that this effect requires activation of NF-κB but not of HIF.
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Effects of hypoxia and oxidative stress on expression of neprilysin in human neuroblastoma cells and rat cortical neurones and astrocytes.
TL;DR: By comparing the effects of hypoxia and oxidative stress on expression and activity of the Aβ-degrading enzyme NEP in human neuroblastoma NB7 cells and rat primary cortical neurones, it is demonstrated thatHypoxia reduced NEP expression at the protein and mRNA levels as well as its activity.
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α-Synuclein modulation of Ca2+ signaling in human neuroblastoma (SH-SY5Y) cells
Nishani T. Hettiarachchi,Andrew Parker,Mark L. Dallas,Kyla Pennington,Chao-Chun Hung,Hugh A. Pearson,John P. Boyle,Philip A. Robinson,Chris Peers +8 more
TL;DR: The findings suggest that α‐syn regulates Ca2+ entry pathways and, consequently, that abnormal α‐ syn levels may promote neuronal damage through dysregulation of Ca2 + homeostasis.
109
Amyloid β peptide as a physiological modulator of neuronal ‘A’-type K+ current
Leigh D. Plant,Nicola J. Webster,John P. Boyle,Martin Ramsden,Darragh B. Freir,Chris Peers,Hugh A. Pearson +6 more
TL;DR: Data show that Aβ is a modulator of Kv4 subunit expression in neurones at both the functional and the molecular level, and is not only involved in Alzheimer pathology, but is also an important physiological regulator of ion channel expression and hence neuronal excitability.
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Carbon monoxide protects against oxidant-induced apoptosis via inhibition of Kv2.1
Mark L. Dallas,John P. Boyle,Carol J. Milligan,Rachael Sayer,Talitha L Kerrigan,Connor McKinstry,Peiyuan Lu,Jamel Mankouri,Mark Harris,Jason L. Scragg,Hugh A. Pearson,Chris Peers +11 more
TL;DR: The results provide a novel mechanism to account for the neuroprotective effects of CO against oxidative apoptosis, which has potential for therapeutic exploitation to provide neuronal protection in situations of oxidative stress.
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