PubMed · 4386537
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B W Barry. 1968. Crystallization in polyhedral emulsion particles.. https://doi.org/10.1111/j.2042-7158.1968.tb09790.x
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Fusel alcohols are natural products of amino acid catabolism in the yeast Saccharomyces cerevisiae that cause morphological changes similar to those seen during pseudohyphal growth. We have discovered that certain of these alcohols, including butanol and isoamyl alcohol, bring about a rapid inhibition of translation at the initiation step. This inhibition is strain specific and is not explained by previously described translational control pathways. Using genetic mapping, we have identified a proline to serine allelic variation at amino acid 180 of the GCD1 gene product as the genetic locus that allows translational regulation upon butanol addition. Gcd1p forms part of the eIF2B guanine nucleotide complex that is responsible for recycling eIF2-GDP to eIF2-GTP. This represents one of the key limiting steps of translation initiation and we provide evidence that fusel alcohols target eIF2B in order to bring about translational regulation.
Estrogens can protect neurons against oxidative stress-induced cell death due to their antioxidant potential. Here, we report that other aromatic alcohols with intact phenolic groups and different phenol derivatives can also protect neurons against oxidative cell death induced by glutamate and hydrogen peroxide in vitro. This neuroprotective activity was independent of the time the compound was added before the toxin. Methylation of the phenolic hydroxyl group led to a decrease or loss in neuroprotection. Moreover, the tested compounds directly inhibited peroxidation reactions, suggesting that neuroprotection is mediated by their antioxidant properties.
1. Phenylephrine (10 microM) evoked rises in tension in isolated rings of endothelium-denuded rabbit superior mesenteric artery. These increases consisted of a tonic component with superimposed rhythmic activity, the frequency of which generally remained constant over time but whose amplitude exhibited cycle-to-cycle variability. 2. The amplitude, but not the frequency, of the rhythmic activity was affected by a series of short peptides possessing sequence homology with extracellular loops 1 and 2 of connexin 43 (Cx43). Oscillatory behaviour was abolished at concentrations of 100-300 microM (IC50 of 20-30 microM), without change in average tone. No synergy was evident between peptides corresponding to the extracellular loops, and cytoplasmic loop peptides were biologically inactive. 3. The putative gap junction inhibitor heptanol mimicked the action of the extracellular loop peptides and abolished rhythmic activity at concentrations of 100-300 microM without effects on frequency. However, in marked contrast to the peptides, heptanol completely inhibited the contraction evoked by phenylephrine (IC50, 283 +/- 28 microM). 4. The presence of mRNA encoding Cx32, Cx40 and Cx43 was detected in the rabbit superior mesenteric artery by reverse transcriptase-polymerase chain reaction. Western blot analysis showed that Cx43 was the major connexin in the endothelium-denuded vessel wall. 5. We conclude that intercellular communication between vascular smooth muscle cells via gap junctions is essential for synchronized rhythmic activity in isolated arterial tissue, whereas tonic force development appears to be independent of cell-cell coupling. The molecular specificity of the peptide probes employed in the study suggests that the smooth muscle relaxant effects of heptanol may be non-specific and unrelated to inhibition of gap junctional communication.