Molecular Rectifier
Mostrando 1-12 de 14 artigos, teses e dissertações.
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1. Retificadores moleculares: transferÃncia autoconsistente de elÃtrons em sistemas doadoraceitador
AtravÃs de cÃlculos ab initio Hartree-Fock e com base na teoria do funcional densidade, esta dissertaÃÃo consiste em um estudo teÃrico sobre os efeitos do campo elÃtrico na estrutura eletrÃnica de um sistema molecular do tipo doador - ponte saturada - aceitador, como parte de uma avaliaÃÃo mais completa de molÃculas que possam servir como dispositi
Publicado em: 2007
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2. A fullerene molecular tip can detect localized and rectified electron tunneling within a single fullerene–porphyrin pair
A fullerene molecular tip was used to detect electron tunneling from a single porphyrin molecule. Electron tunneling was found to occur locally from an electron-donating moiety of the porphyrin to the fullerene through charge-transfer interaction between them. In addition, electron tunneling within the single fullerene–porphyrin pair exhibited rectifying b
National Academy of Sciences.
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3. Alternative splicing contributes to K+ channel diversity in the mammalian central nervous system.
In an attempt to define the molecular basis of the functional diversity of K+ channels, we have isolated overlapping rat brain cDNAs that encoded a neuronal delayed rectifier K+ channel, K,4, that is structurally related to the Drosophila Shaw protein. Unlike previously characterized mammalian K+ channel genes, which each contain a single protein-coding exon
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4. Molecular basis for the inhibition of G protein-coupled inward rectifier K+ channels by protein kinase C
G protein-coupled inward rectifier K+ (GIRK) channels regulate cellular excitability and neurotransmission. The GIRK channels are activated by a number of inhibitory neurotransmitters through the G protein βγ subunit (Gβγ) after activation of G protein-coupled receptors and inhibited by several excitatory neurotransmitters through activation of phospholi
National Academy of Sciences.
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5. Molecular basis of cardiac potassium channel stimulation by protein kinase A.
Cardiac beta-adrenergic receptors accelerate heart rate by modulating ionic currents through a pathway involving cyclic AMP-dependent protein kinase A (PKA). Previous studies have focused on the regulation of Ca2+ channels by PKA; however, due to the heterogeneity of K+ channels expressed within the heart, little is known about the mechanism by which PKA mod
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6. Molecular cloning of a member of a third class of Shaker-family K+ channel genes in mammals.
We report the cloning of RKShIIIA, a cDNA encoding a K+ channel sequence expressed in rat brain. This cDNA encodes K+ channel subunits that express in Xenopus oocytes a slow, 4-aminopyridine- and tetraethylammonium-sensitive, delayed rectifier-type K+ channel activated by large membrane depolarizations. This gene belongs to the Shaker (Sh) family of K+ chann
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7. Electrophysiological properties of neonatal mouse cardiac myocytes in primary culture.
1. The increasing utility of transgenic mice in molecular studies of the cardiovascular system has motivated us to characterize the ionic currents in neonatal mouse ventricular myocytes. 2. Cell capacitance measurements (30 +/- 1 pF, n = 73) confirmed visual impressions that neonatal mouse ventricular myocytes in primary culture are considerably smaller than
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8. Regulation of ROMK1 channel by protein kinase A via a phosphatidylinositol 4,5-bisphosphate-dependent mechanism
ROMK inward-rectifier K+ channels control renal K+ secretion. The activity of ROMK is regulated by protein kinase A (PKA), but the molecular mechanism for regulation is unknown. Having found that direct interaction with membrane phosphatidylinositol 4,5-bisphosphate (PIP2) is essential for channel activation, we investigate here the role of PIP2 in regulatio
The National Academy of Sciences.
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9. Molecular determinants for activation and inactivation of HERG, a human inward rectifier potassium channel.
1. The human eag-related potassium channel, HERG, gives rise to inwardly rectifying K+ currents when expressed in Xenopus oocytes. 2. The apparent inward rectification is caused by rapid inactivation. In extracellular Cs+ solutions, large outward currents can be recorded having an inactivation time constant at 0 mV of about 50 ms with an e-fold change every
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10. Molecular identification of the role of voltage-gated K+ channels, Kv1.5 and Kv2.1, in hypoxic pulmonary vasoconstriction and control of resting membrane potential in rat pulmonary artery myocytes.
Hypoxia initiates pulmonary vasoconstriction (HPV) by inhibiting one or more voltage-gated potassium channels (Kv) in the pulmonary artery smooth muscle cells (PASMCs) of resistance arteries. The resulting membrane depolarization increases opening of voltage-gated calcium channels, raising cytosolic Ca2+ and initiating HPV. There are presently nine families
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11. pH gating of ROMK (Kir1.1) channels: Control by an Arg-Lys-Arg triad disrupted in antenatal Bartter syndrome
Inward-rectifier K+ channels of the ROMK (Kir1.1) subtype are responsible for K+ secretion and control of NaCl absorption in the kidney. A hallmark of these channels is their gating by intracellular pH in the neutral range. Here we show that a lysine residue close to TM1, identified previously as a structural element required for pH-induced gating, is proton
The National Academy of Sciences.
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12. Heteromerization of Kir2.x potassium channels contributes to the phenotype of Andersen's syndrome
Andersen's syndrome, an autosomal dominant disorder related to mutations of the potassium channel Kir2.1, is characterized by cardiac arrhythmias, periodic paralysis, and dysmorphic bone structure. The aim of our study was to find out whether heteromerization of Kir2.1 channels with wild-type Kir2.2 and Kir2.3 channels contributes to the phenotype of Anderse
The National Academy of Sciences.