The Experts below are selected from a list of 279 Experts worldwide ranked by ideXlab platform
Adriano Senatore - One of the best experts on this subject based on the ideXlab platform.
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a na leak channel cloned from trichoplax adhaerens extends extracellular ph and ca2 sensing for the deg enac family close to the base of metazoa
Journal of Biological Chemistry, 2019Co-Authors: Wassim Elkhatib, Carolyn L Smith, Adriano SenatoreAbstract:Acid-sensitive ion channels belonging to the degenerin/epithelial sodium channel (DEG/ENaC) family activate in response to extracellular Protons and are considered unique to deuterostomes. However, sensitivity to pH/Protons is more widespread, where, for example, human ENaC Na+ leak channels are potentiated and mouse BASIC and Caenorhabditis elegans ACD-1 Na+ leak channels are blocked by extracellular Protons. For many DEG/ENaC channels, extracellular Ca2+ ions modulate gating, and in some cases, the binding of Protons and Ca2+ is interdependent. Here, we functionally characterize a DEG/ENaC channel from the early-diverging animal Trichoplax adhaerens, TadNaC6, that conducts Na+-selective leak currents in vitro sensitive to blockade by both extracellular Protons and Ca2+. We determine that proton block is enhanced in low external Ca2+ concentration, whereas calcium block is enhanced in low external proton concentration, indicative of competitive binding of these two ligands to extracellular sites of the channel protein. TadNaC6 lacks most determinant residues for proton and Ca2+ sensitivity in other DEG/ENaC channels, and a mutation of one conserved residue (S353A) associated with Ca2+ block in rodent BASIC channels instead affected proton sensitivity, all indicative of independent evolution of H+ and Ca2+ sensitivity. Strikingly, TadNaC6 was potently activated by the general DEG/ENaC channel blocker amiloride, a rare feature only reported for the acid-activated channel ASIC3. The sequence and structural divergence of TadNaC6, coupled with its noncanonical functional features, provide unique opportunities for probing the proton, Ca2+, and amiloride regulation of DEG/ENaC channels and insight into the possible core-gating features of ancestral ion channels.
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A Na+ leak channel cloned from Trichoplax adhaerens extends extracellular pH and Ca2+ sensing for the DEG/ENaC family close to the base of Metazoa.
The Journal of biological chemistry, 2019Co-Authors: Wassim Elkhatib, Carolyn L Smith, Adriano SenatoreAbstract:Acid-sensitive ion channels belonging to the degenerin/epithelial sodium channel (DEG/ENaC) family activate in response to extracellular Protons and are considered unique to deuterostomes. However, sensitivity to pH/Protons is more widespread, where, for example, human ENaC Na+ leak channels are potentiated and mouse BASIC and Caenorhabditis elegans ACD-1 Na+ leak channels are blocked by extracellular Protons. For many DEG/ENaC channels, extracellular Ca2+ ions modulate gating, and in some cases, the binding of Protons and Ca2+ is interdependent. Here, we functionally characterize a DEG/ENaC channel from the early-diverging animal Trichoplax adhaerens, TadNaC6, that conducts Na+-selective leak currents in vitro sensitive to blockade by both extracellular Protons and Ca2+ We determine that proton block is enhanced in low external Ca2+ concentration, whereas calcium block is enhanced in low external proton concentration, indicative of competitive binding of these two ligands to extracellular sites of the channel protein. TadNaC6 lacks most determinant residues for proton and Ca2+ sensitivity in other DEG/ENaC channels, and a mutation of one conserved residue (S353A) associated with Ca2+ block in rodent BASIC channels instead affected proton sensitivity, all indicative of independent evolution of H+ and Ca2+ sensitivity. Strikingly, TadNaC6 was potently activated by the general DEG/ENaC channel blocker amiloride, a rare feature only reported for the acid-activated channel ASIC3. The sequence and structural divergence of TadNaC6, coupled with its noncanonical functional features, provide unique opportunities for probing the proton, Ca2+, and amiloride regulation of DEG/ENaC channels and insight into the possible core-gating features of ancestral ion channels.
Qianli Chen - One of the best experts on this subject based on the ideXlab platform.
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experimental neutron scattering evidence for proton polaron in hydrated metal oxide proton conductors
Nature Communications, 2017Co-Authors: Qianli ChenAbstract:Hydration of oxygen vacancies could form hydroxyl groups with interstitial structural Protons. Here a quasi-elastic neutron scattering study reveals proton polarons in proton-conducting ceramic electrolytes, and the proton transport turns out to be a cooperative process.…
J C Kasper - One of the best experts on this subject based on the ideXlab platform.
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self consistent ion cyclotron anisotropy beta relation for solar wind Protons
The Astrophysical Journal, 2013Co-Authors: Philip A Isenberg, Bennett A Maruca, J C KasperAbstract:We derive a set of self-consistent marginally stable states for a system of ion-cyclotron waves propagating parallel to the large-scale magnetic field through a homogeneous proton-electron plasma. The proton distributions and the wave dispersions are related through the condition that no further ion-cyclotron resonant particle scattering or wave growth/damping may take place. The thermal anisotropy of the Protons in these states therefore defines the threshold value for triggering the proton-cyclotron anisotropy instability. A number of recent papers have noted that the anisotropy of solar wind Protons at 1 AU does not seem to be limited by the proton-cyclotron anisotropy threshold, even at low plasma beta. However, this puzzle seems to be due solely to the estimation of this anisotropy threshold under the assumption that the Protons have a bi-Maxwellian distribution. We note that bi-Maxwellian distributions are never marginally stable to the resonant cyclotron interaction, so these estimates do not represent physically valid thresholds. The threshold anisotropies obtained from our marginally stable states are much larger, as a function of proton parallel beta, than the bi-Maxwellian estimates, and we show that the measured data remains below these more rigorous thresholds. Thus, the results of this paper resolve the apparent contradiction presented by the solar wind anisotropy observations at 1 AU: the bi-Maxwellian anisotropies are not rigorous thresholds, and so do not limit the proton distributions in the solar wind.
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self consistent ion cyclotron anisotropy beta relation for solar wind Protons
SOLAR WIND 13: Proceedings of the Thirteenth International Solar Wind Conference, 2013Co-Authors: Philip A Isenberg, Bennett A Maruca, J C KasperAbstract:Proton distributions with perpendicular anisotropies above a beta-dependent threshold trigger the quasilinear proton cyclotron instability, causing the generation of ion cyclotron waves and the scattering of Protons to lower anisotropy. However, observations of solar wind proton distributions at 1 AU imply that this instability is ineffective in limiting the proton anisotropy. Here, we resolve this puzzle. We first point out that the commonly used estimates of the ion cyclotron threshold are based on bi-Maxwellians which are never marginally stable. Second, we derive a self-consistent marginally stable state of Protons and parallel ion cyclotron waves which yields true threshold anisotropies which do in fact bound the solar wind data.
Wassim Elkhatib - One of the best experts on this subject based on the ideXlab platform.
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a na leak channel cloned from trichoplax adhaerens extends extracellular ph and ca2 sensing for the deg enac family close to the base of metazoa
Journal of Biological Chemistry, 2019Co-Authors: Wassim Elkhatib, Carolyn L Smith, Adriano SenatoreAbstract:Acid-sensitive ion channels belonging to the degenerin/epithelial sodium channel (DEG/ENaC) family activate in response to extracellular Protons and are considered unique to deuterostomes. However, sensitivity to pH/Protons is more widespread, where, for example, human ENaC Na+ leak channels are potentiated and mouse BASIC and Caenorhabditis elegans ACD-1 Na+ leak channels are blocked by extracellular Protons. For many DEG/ENaC channels, extracellular Ca2+ ions modulate gating, and in some cases, the binding of Protons and Ca2+ is interdependent. Here, we functionally characterize a DEG/ENaC channel from the early-diverging animal Trichoplax adhaerens, TadNaC6, that conducts Na+-selective leak currents in vitro sensitive to blockade by both extracellular Protons and Ca2+. We determine that proton block is enhanced in low external Ca2+ concentration, whereas calcium block is enhanced in low external proton concentration, indicative of competitive binding of these two ligands to extracellular sites of the channel protein. TadNaC6 lacks most determinant residues for proton and Ca2+ sensitivity in other DEG/ENaC channels, and a mutation of one conserved residue (S353A) associated with Ca2+ block in rodent BASIC channels instead affected proton sensitivity, all indicative of independent evolution of H+ and Ca2+ sensitivity. Strikingly, TadNaC6 was potently activated by the general DEG/ENaC channel blocker amiloride, a rare feature only reported for the acid-activated channel ASIC3. The sequence and structural divergence of TadNaC6, coupled with its noncanonical functional features, provide unique opportunities for probing the proton, Ca2+, and amiloride regulation of DEG/ENaC channels and insight into the possible core-gating features of ancestral ion channels.
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A Na+ leak channel cloned from Trichoplax adhaerens extends extracellular pH and Ca2+ sensing for the DEG/ENaC family close to the base of Metazoa.
The Journal of biological chemistry, 2019Co-Authors: Wassim Elkhatib, Carolyn L Smith, Adriano SenatoreAbstract:Acid-sensitive ion channels belonging to the degenerin/epithelial sodium channel (DEG/ENaC) family activate in response to extracellular Protons and are considered unique to deuterostomes. However, sensitivity to pH/Protons is more widespread, where, for example, human ENaC Na+ leak channels are potentiated and mouse BASIC and Caenorhabditis elegans ACD-1 Na+ leak channels are blocked by extracellular Protons. For many DEG/ENaC channels, extracellular Ca2+ ions modulate gating, and in some cases, the binding of Protons and Ca2+ is interdependent. Here, we functionally characterize a DEG/ENaC channel from the early-diverging animal Trichoplax adhaerens, TadNaC6, that conducts Na+-selective leak currents in vitro sensitive to blockade by both extracellular Protons and Ca2+ We determine that proton block is enhanced in low external Ca2+ concentration, whereas calcium block is enhanced in low external proton concentration, indicative of competitive binding of these two ligands to extracellular sites of the channel protein. TadNaC6 lacks most determinant residues for proton and Ca2+ sensitivity in other DEG/ENaC channels, and a mutation of one conserved residue (S353A) associated with Ca2+ block in rodent BASIC channels instead affected proton sensitivity, all indicative of independent evolution of H+ and Ca2+ sensitivity. Strikingly, TadNaC6 was potently activated by the general DEG/ENaC channel blocker amiloride, a rare feature only reported for the acid-activated channel ASIC3. The sequence and structural divergence of TadNaC6, coupled with its noncanonical functional features, provide unique opportunities for probing the proton, Ca2+, and amiloride regulation of DEG/ENaC channels and insight into the possible core-gating features of ancestral ion channels.
Carolyn L Smith - One of the best experts on this subject based on the ideXlab platform.
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a na leak channel cloned from trichoplax adhaerens extends extracellular ph and ca2 sensing for the deg enac family close to the base of metazoa
Journal of Biological Chemistry, 2019Co-Authors: Wassim Elkhatib, Carolyn L Smith, Adriano SenatoreAbstract:Acid-sensitive ion channels belonging to the degenerin/epithelial sodium channel (DEG/ENaC) family activate in response to extracellular Protons and are considered unique to deuterostomes. However, sensitivity to pH/Protons is more widespread, where, for example, human ENaC Na+ leak channels are potentiated and mouse BASIC and Caenorhabditis elegans ACD-1 Na+ leak channels are blocked by extracellular Protons. For many DEG/ENaC channels, extracellular Ca2+ ions modulate gating, and in some cases, the binding of Protons and Ca2+ is interdependent. Here, we functionally characterize a DEG/ENaC channel from the early-diverging animal Trichoplax adhaerens, TadNaC6, that conducts Na+-selective leak currents in vitro sensitive to blockade by both extracellular Protons and Ca2+. We determine that proton block is enhanced in low external Ca2+ concentration, whereas calcium block is enhanced in low external proton concentration, indicative of competitive binding of these two ligands to extracellular sites of the channel protein. TadNaC6 lacks most determinant residues for proton and Ca2+ sensitivity in other DEG/ENaC channels, and a mutation of one conserved residue (S353A) associated with Ca2+ block in rodent BASIC channels instead affected proton sensitivity, all indicative of independent evolution of H+ and Ca2+ sensitivity. Strikingly, TadNaC6 was potently activated by the general DEG/ENaC channel blocker amiloride, a rare feature only reported for the acid-activated channel ASIC3. The sequence and structural divergence of TadNaC6, coupled with its noncanonical functional features, provide unique opportunities for probing the proton, Ca2+, and amiloride regulation of DEG/ENaC channels and insight into the possible core-gating features of ancestral ion channels.
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A Na+ leak channel cloned from Trichoplax adhaerens extends extracellular pH and Ca2+ sensing for the DEG/ENaC family close to the base of Metazoa.
The Journal of biological chemistry, 2019Co-Authors: Wassim Elkhatib, Carolyn L Smith, Adriano SenatoreAbstract:Acid-sensitive ion channels belonging to the degenerin/epithelial sodium channel (DEG/ENaC) family activate in response to extracellular Protons and are considered unique to deuterostomes. However, sensitivity to pH/Protons is more widespread, where, for example, human ENaC Na+ leak channels are potentiated and mouse BASIC and Caenorhabditis elegans ACD-1 Na+ leak channels are blocked by extracellular Protons. For many DEG/ENaC channels, extracellular Ca2+ ions modulate gating, and in some cases, the binding of Protons and Ca2+ is interdependent. Here, we functionally characterize a DEG/ENaC channel from the early-diverging animal Trichoplax adhaerens, TadNaC6, that conducts Na+-selective leak currents in vitro sensitive to blockade by both extracellular Protons and Ca2+ We determine that proton block is enhanced in low external Ca2+ concentration, whereas calcium block is enhanced in low external proton concentration, indicative of competitive binding of these two ligands to extracellular sites of the channel protein. TadNaC6 lacks most determinant residues for proton and Ca2+ sensitivity in other DEG/ENaC channels, and a mutation of one conserved residue (S353A) associated with Ca2+ block in rodent BASIC channels instead affected proton sensitivity, all indicative of independent evolution of H+ and Ca2+ sensitivity. Strikingly, TadNaC6 was potently activated by the general DEG/ENaC channel blocker amiloride, a rare feature only reported for the acid-activated channel ASIC3. The sequence and structural divergence of TadNaC6, coupled with its noncanonical functional features, provide unique opportunities for probing the proton, Ca2+, and amiloride regulation of DEG/ENaC channels and insight into the possible core-gating features of ancestral ion channels.
