Biochimica et biophysica acta最新文献

The Publisher regrets that this article is an accidental duplication of an article that has already been published in Biochem. Biophys. Acta, doi:10.1016/j.bbagrm.2007.09.001. The duplicate article has therefore been withdrawn.

The Publisher regrets that this article is an accidental duplication of an article that has already been published in Biochem. Biophys. Acta, doi:10.1016/j.bbagrm.2007.09.002. The duplicate article has therefore been withdrawn.

The Publisher regrets that this article is an accidental duplication of an article that has already been published in Biochem. Biophys. Acta, doi:10.1016/j.bbagrm.2007.09.003. The duplicate article has therefore been withdrawn.

The Publisher regrets that this article is an accidental duplication of an article that has already been published in Biochem. Biophys. Acta, doi:10.1016/j.bbagrm.2007.09.004. The duplicate article has therefore been withdrawn.

The Publisher regrets that this article is an accidental duplication of an article that has already been published in Biochim. Biophys. Acta, doi:10.1016/j.bbagrm.2007.08.001. The duplicate article has therefore been withdrawn.

The Golgi apparatus in animal cells breaks down at the onset of mitosis and is later rebuilt in the two daughter cells. Two AAA ATPases, NSF and p97/VCP, have been implicated in regulating membrane fusion steps that lead to regrowth of Golgi cisternae from mitotic fragments. NSF dissociates complexes of SNARE proteins, thereby reactivating them to mediate membrane fusion. However, NSF has a second function in regulating SNARE pairing together with the ubiquitin-like protein GATE-16. p97/VCP, on the other hand, is involved in a cycle of ubiquitination and deubiquitination of an unknown target that governs Golgi membrane dynamics. Here, these findings are reviewed and discussed in the context of the increasingly evident role of ubiquitin in membrane traffic processes.

SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) are now generally accepted to be the major players in the final stage of the docking and the subsequent fusion of diverse vesicle-mediated transport events. The SNARE-mediated process is conserved evolutionally from yeast to human, as well as mechanistically and structurally across different transport events in eukaryotic cells. In the post-genomic era, a fairly complete list of "all" SNAREs in several organisms (including human) can now be made. This review aims to summarize the key properties and the mechanism of action of SNAREs in mammalian cells.

The results of several experimental and epidemiological studies have shown an inverse correlation between Mg status and the risk of some cancers. However, relationship between magnesium and cancer is complex. The aim of our work was to examine the precise effect of Mg deficiency on transplantable mouse tumor growth and metastasis. The results obtained indicate a significant retardation of primary tumor growth (up to 70%) in mice receiving Mg-deficient diet. However, Mg repletion caused in these mice significant increase of primary tumor burden. Analysis of cell cycle distribution showed a reduced percentage of cells in the S phase and an increase of cells in the G(0)/G(1) phase of the cell cycle in LLC tumors caused by Mg deficiency. This is in agreement with the effect of low Mg level on cell growth observed in vitro. Interestingly, in mice inoculated with LLC cells and receiving low-magnesium diet, a higher metastatic potential was observed as compared to control mice. In conclusion, our results demonstrate a direct role of magnesium in tumor growth and also point at deleterious effect of low magnesium status on tumor metastasis.