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A. De Vuyst G. Thinès L. Henriet M. Soffié 《Cellular and molecular life sciences : CMLS》1964,20(11):648-650
Summary In a preliminary series of experiments, it was noted that dairy bulls who refused to mount the cow for a long time, could be induced to mount it again when acoustically stimulated by specific calls of cows emitted by a magnetophone. In these conditions, the reaction time of the bulls was also shorter, while ejaculated quantities did not differ from those obtained before the experiments. It is suggested that this rather simple procedure could be helpful when the use of bulls as teasers raises difficulties. 相似文献
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J. -M. Pérès 《Cellular and molecular life sciences : CMLS》1947,3(8):330-331
Sans résumé 相似文献
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Copper is a cofactor for many cellular enzymes and transporters. It can be loaded onto secreted and endomembrane cuproproteins by translocation from the cytosol into membrane-bound organelles by ATP7A or ATP7B transporters, the genes for which are mutated in the copper imbalance syndromes Menkes disease and Wilson disease, respectively. Endomembrane cuproproteins are thought to incorporate copper stably on transit through the trans-Golgi network, in which ATP7A accumulates by dynamic cycling through early endocytic compartments. Here we show that the pigment-cell-specific cuproenzyme tyrosinase acquires copper only transiently and inefficiently within the trans-Golgi network of mouse melanocytes. To catalyse melanin synthesis, tyrosinase is subsequently reloaded with copper within specialized organelles called melanosomes. Copper is supplied to melanosomes by ATP7A, a cohort of which localizes to melanosomes in a biogenesis of lysosome-related organelles complex-1 (BLOC-1)-dependent manner. These results indicate that cell-type-specific localization of a metal transporter is required to sustain metallation of an endomembrane cuproenzyme, providing a mechanism for exquisite spatial control of metalloenzyme activity. Moreover, because BLOC-1 subunits are mutated in subtypes of the genetic disease Hermansky-Pudlak syndrome, these results also show that defects in copper transporter localization contribute to hypopigmentation, and hence perhaps other systemic defects, in Hermansky-Pudlak syndrome. 相似文献