FEBS letters
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A number of disorders related to cystic fibrosis have been described since the cloning of the cystic fibrosis gene, including infertility due to the congenital bilateral absence of the vas deferens. We have identified, in several patients, complex cystic fibrosis transmembrane conductance regulator genotypes like double-mutant alleles. ⋯ We found that R74W cystic fibrosis transmembrane conductance regulator appears to be a polymorphism, while D1270N cystic fibrosis transmembrane conductance regulator could be responsible for the congenital bilateral absence of the vas deferens phenotype. The combination of the two produced a more severe effect on the chloride conductance pathway as well as on the phenotype.
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Localization of the mRNAs for fractalkine, a CX3C chemokine, and for its receptor CX3CR1 was investigated in the rat brain. In situ hybridization study revealed that fractalkine mRNA was dominantly expressed in neuronal cells particularly in the olfactory bulb, cerebral cortex, hippocampus, caudate putamen and nucleus accumbens. ⋯ The in vitro study suggested the cells expressing CX3CR1 mRNA are microglia, not astrocytes or neurons. Fractalkine appears to function as a signal molecule from neuron to microglia.
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G protein-activated inwardly rectifying K+ channel subunits GIRK1 (Kir 3.1), GIRK2 (Kir 3.2), and CIR (Kir 3.4) were expressed individually or in combination in Xenopus oocytes and CHO cells. GIRK1 coexpressed with CIR or GIRK2, produced currents up to 10-fold larger than any of the subunits expressed alone. No such clear synergistic effects were observed upon coexpression of CIR/GIRK2 under the same conditions. ⋯ The single GIRK1/GIRK2 channels resembled previously described neuronal G protein-gated K+ channels. In contrast, single GIRK2 channels were short-lived and unlike any previously described neuronal K+ channel. We propose that some neuronal G protein-activated inward rectifier K+ channels may be formed by a GIRK1/GIRK2 heteromultimer and that G beta gamma activation may involve both subunits.