A Model for Manganese interaction with Deinococcus radiodurans proteome network involved in ROS response and defense.

A complex network of regulatory proteins takes part in the mechanism underlying the radioresistance of Deinoccocus radiodurans bacterium (DR). The interaction of Mn(II) ions with DR-proteins and peptides seems to be responsible for proteins protection from oxidative damage induced by Reactive Oxygen Species during irradiation. In the present work we describe a combined approach of bioinformatic strategies based on structural data and annotation to predict the Mn(II)-binding proteins encoded by the genome of DR and, in parallel, the same predictions for other bacteria were performed; the comparison revealed that, in most of the cases, the content of Mn(II)-binding proteins is significantly higher in radioresistant than in radiosensitive bacteria.

Ni(II) interaction with a peptide model of the human TLR4 ectodomain.

Ni(II) stimulates innate immunity via the direct binding to human Toll Like Receptor 4 (hTLR4), the bacterial lypopolysaccharide receptor. The binding is specific for humans and causes nickel contact allergy. The protein sequence analysis of hTLR4 revealed that the ectodomain, the region supposed to coordinate the metal ions, contains a histidine-rich motif that is not conserved among all organisms.

Early phagocytosis of glucose-6-phosphate dehydrogenase (G6PD)-deficient erythrocytes parasitized by Plasmodium falciparum may explain malaria protection in G6PD deficiency.

In population-based studies it has been established that inherited deficiency of erythrocyte (E) glucose-6-phosphate dehydrogenase (G6PD) confers protection against severe Plasmodium falciparum (P falciparum) malaria. Impaired growth of parasites in G6PD-deficient E in vitro has been reported in some studies, but not in others. In a systematic analysis, we have found that with five different strains of P falciparum (FCR-3, KI, C10, HB3B, and T9/96), there was no significant difference in either invasion or maturation when the parasites were grown in either normal or G6PD-deficient (Mediterranean variant) E.