pH regulation and beyond: unanticipated functions for the voltage-gated proton channel, HVCN1

Capasso, Melania; DeCoursey, Thomas E.; Dyer, Martin J. S.

doi:10.1016/j.tcb.2010.09.006

Cited by 82 publications

(91 citation statements)

References 86 publications

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“…Preeminent examples include ATP oxidative phosphorylation in mithochondria 2 , the HCVN1 voltage-gated proton channel 3 , light-activated proton pumping in bacteriorhodopsin 4 , and the proton-conducting single water file in the antibiotic gramicidin 5 . In living systems, electrical signals are communicated and processed by modulating ionic 6 and protonic currents 7 .…”

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confidence: 99%

A polysaccharide bioprotonic field-effect transistor

et al. 2011

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In nature, electrical signalling occurs with ions and protons, rather than electrons. Artificial devices that can control and monitor ionic and protonic currents are thus an ideal means for interfacing with biological systems. Here we report the first demonstration of a biopolymer protonic field-effect transistor with proton-transparent PdH x contacts. In maleic-chitosan nanofibres, the flow of protonic current is turned on or off by an electrostatic potential applied to a gate electrode. The protons move along the hydrated maleic-chitosan hydrogen-bond network with a mobility of ~4. . This study introduces a new class of biocompatible solid-state devices, which can control and monitor the flow of protonic current. This represents a step towards bionanoprotonics.

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confidence: 99%

A polysaccharide bioprotonic field-effect transistor

et al. 2011

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“…While the protons produced by metabolism contribute little to extracellular proton signaling, a burst of proton release, which can occur under specific conditions such as muscle contraction and activation of leukocytes by pathogens [17] , may function beyond metabolism. During infection or inflammation in the mammalian brain, activated microglia and other neutrophils can also generate a proton burst through the NADPH oxidase complex [18] . The protons generated are then extruded to the extracellular space by Hv1 proton channels to kill the bacteria engulfed by phagocytes [18,19] .…”

Section: De Novo Proton-generating Pathways and Their Pathophysiologimentioning

confidence: 99%

“…During infection or inflammation in the mammalian brain, activated microglia and other neutrophils can also generate a proton burst through the NADPH oxidase complex [18] . The protons generated are then extruded to the extracellular space by Hv1 proton channels to kill the bacteria engulfed by phagocytes [18,19] .…”

Section: De Novo Proton-generating Pathways and Their Pathophysiologimentioning

confidence: 99%

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Proton production, regulation and pathophysiological roles in the mammalian brain

Zeng

2012

Neurosci. Bull.

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Abstract:The recent demonstration of proton signaling in C. elegans muscle contraction suggests a novel mechanism for proton-based intercellular communication and has stimulated enthusiasm for exploring proton signaling in higher organisms. Emerging evidence indicates that protons are produced and regulated in localized space and time. Furthermore, identification of proton regulators and sensors in the brain leads to the speculation that proton production and regulation may be of major importance for both physiological and pathological functions ranging from nociception to learning and memory. Extracellular protons may play a role in signal transmission by not only acting on adjacent cells but also affecting the cell from which they were released. In this review, we summarize the upstream and downstream pathways of proton production and regulation in the mammalian brain, with special emphasis on the proton extruders and sensors that are critical in the homeostatic regulation of pH, and discuss their potential roles in proton signaling under normal and pathophysiological conditions.

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“…In B cells however, proton channels play a cell signaling role, because H 2 O 2 diffuses back across the B-cell membrane to oxidize and inactivate SHP-1, a protein tyrosine phosphatase that negatively regulates the signaling cascade initiated by the binding of antigens to the B cell receptor (Capasso et al, 2010). By inhibiting the activity of SHP-1 and preventing it from dephosphorylating the protein tyrosine kinase Syk, Hv1 channels amplify BCR signaling, thereby boosting the expression of several genes involved in B cell proliferation, differentiation, and immunoglobulin production (Capasso et al, 2011).…”

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Do Hv1 proton channels regulate the ionic and redox homeostasis of phagosomes?

Chemaly

Demaurex

2012

Molecular and Cellular Endocrinology

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a b s t r a c tRecent work on animal models has revealed the important role played by the voltage-gated proton channel Hv1 during bacterial killing by innate immune cells. Studies from mice lacking Hv1 channels showed that Hv1 proton channels are required for high-level production of reactive oxygen species (ROS) by the NADPH oxidase of phagocytes (NOX2) in two ways. First, Hv1 channels maintain a physiological membrane potential during the respiratory burst of neutrophils by providing a compensating charge for the electrons transferred by NOX2 from NADPH to superoxide. Second, Hv1 channels maintain a physiological cytosolic pH by extruding the acid generated by the NOX2-dependent consumption of NADPH. The two mechanisms directly sustain the activity of the NOX2 enzyme and indirectly sustain other neutrophil functions by enhancing the driving force for the entry of calcium into cells, thereby boosting cellular calcium signals. The increased depolarization of Hv1-deficient neutrophils aborted calcium responses to chemoattractants and revealed adhesion and migration defects that were associated with an impaired depolymerization of the cortical actin cytoskeleton. Current research aims to transpose these findings to phagosomes, the phagocytic vacuoles where bacterial killing takes place. However, the mechanisms that control the phagosomal pH appear to vary greatly between phagocytes: phagosomes rapidly acidify in macrophages but remain neutral for several minutes in neutrophils following ingestion of solid particles, whereas in dendritic cells phagosomes alkalinize, a mechanism thought to promote antigen crosspresentation. In this review, we discuss how the knowledge gained on the role of Hv1 channels at the plasma membrane of neutrophils can be used to study the regulation of the phagosomal pH, ROS, membrane potential, and calcium fluxes in different phagocytic cells.

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pH regulation and beyond: unanticipated functions for the voltage-gated proton channel, HVCN1

Cited by 82 publications

References 86 publications

A polysaccharide bioprotonic field-effect transistor

A polysaccharide bioprotonic field-effect transistor

Proton production, regulation and pathophysiological roles in the mammalian brain

Do Hv1 proton channels regulate the ionic and redox homeostasis of phagosomes?

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