Human Protein C inhibits selectin-mediated cell adhesion: role of unique fucosylated oligosaccharide

The human anticoagulant factor, Protein C, is a plasma glycoproteinthat has reported anti-ischaemic and anti-inflammatory properties.To explore potential mechanisms for these reported activities,we examined the effect of Protein C on the process of cell adhesionto vascular endothelial cells, which plays a critical role duringinflammatory responses. We show that both human plasma-derivedand human cell-produced recombinant Protein C inhibit E-selectin-mediatedcell adhesion. This effect was not mediated through the serineprotease activity of Protein C, but through its carbohydrates.Using oligosaccharides isolated from human cell-produced ProteinC, we have defined a polylactosamine structural determinantthat inhibits adhesion. This uncharged detenminant appears tobe a more potent ligand for E-selectin than the sialylated LewisX antigen. Our data suggest a potential mechanism for the reportedanti-inflammatory effects of Protein C and describe a new ligandfor selectin-mediated adhesion. cell adhesion fucosylated oligosaccharide human Protein C/PC-293 determinant selectin     

Coordination of phage genome degradation versus host genome protection by a bifunctional restriction-modification enzyme visualized by CryoEM

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Behaviors associated with tube-sharing in Microdeutopus gryllotalpa (Costa) (Crustacea:Amphipoda)

An earlier study showed that the onset of precopulatory behavior, or tube-sharing, in the amphipod crustacean Microdeutopus gryllotalpa (Costa) generally occurred toward the end of the females' intermolt period. Tube-sharing ended when the female molted and copulation occurred. It was hypothesized that after copulation the male would leave the female's tube, travel to another receptive female's tube, and begin tube-sharing with the new female (the “cruising male hypothesis”).The present study confirms this hypothesis for laboratory cultures. In addition, the study describes a female-typical and male-specific behavior (“blocking” and “intermittent pleopod beats”). These behaviors are only expressed during interactions between one individual who is entering, and another individual who is residing in the tube.     

Expression of foreign epitopes in P-fimbriae of Escherichia coli.

Summary Hypervariable regions (HRs) of the major subunit of F11 fimbriae were exploited for insertion of foreign epitopes. Two insertion vectors were created that contain a unique cloning site in HR1 or HR4 respectively. Several oligonucleotides, coding for antigenic determinants derived from different pathogens, were cloned in both insertion vectors. Hybrid fimbrial subunits were generally shown to be assembled in fimbriae when the length of the inserted peptide did not exceed 14 amino acids. The inserted peptides appeared to be exposed in the fimbrial filament. One hybrid fimbrial protein induced detectable levels of antibodies against the inserted epitope if injected into mice.     

Role of plasma membrane redox activities in elongation growth in plants

Comparing isolated plasma membrane vesicles and excised hypocotyl segments from etiolated seedlings of soybean [ Glycine max (L.) Merr. cv. Williams], certain antiproliferative agents that inhibited growth inhibited plasma membrane redox activities. Additionally, auxins that stimulated growth stimulated plasma membrane redox activities. Hormone stimulation was restricted to NADH oxidase (determined from disappearance of NADH) and was given both by isolated plasma membranes and by a soluhilizedenzyme preparation. Comparing IAA, the native auxin regulator, and 2,4-D, a synthetic regulator, stimulation was observed, hut the dose-response curves were different. Yet, the dose-response relationships of both stimulation of auxin growth and stimulation of NADH oxidase were parallel. Inhibition of auxin-induced growth by antiproliferative drugs was more complex. Some, like actinomycin D, preferentially inhibited NADH oxidase (EC 1.6.99.2) but inhibited NADH-ferricya-nide oxido-reductase (EC 1.6.99.3) as well. Others, like adriamycin, inhibited primarily the NADH-ferricyanide oxido-reductase. Therefore, growth control by auxin appeared to involve NADH oxidase as a rate-limiting terminal oxidase to link electron flow from NADH to oxygen. This observation may provide a fundamental difference from animal cells. With the latter, impermeant electron acceptors such as diferric transferrin or ferricyanide fulfill such a role. In plants, these impermeant electron acceptors were without effect on growth or were growth inhibitory.     

Distribution of DNA Sequences Encoding Narrow- and Broad-Spectrum Mercury Resistance

The distribution of DNA sequences homologous with three mer genes was determined in unselected and mercury-resistant water and sediment isolates. The maximum proportions of unselected bacterial isolates containing DNA hybridizing with the 358merA, 358merB, and 501merR probes, derived from gram-negative organisms, were 93.8, 21, and 100%, respectively. Up to 53.3% of mercury chloride-resistant isolates and 54% of methylmercury hydroxide-resistant isolates did not contain DNA homologous with 358merA or 358merB, respectively. Hybridizations performed at high and low stringencies demonstrated that divergence of the merA gene accounted for many of the mercury-resistant but probe-negative isolates. Sixteen mercury-resistant Bacillus spp. isolated from the least contaminated site all contained DNA homologous with 258merA, originally from a gram-positive organism, but only four hybridized weakly with 358merA. The results demonstrate the wide distribution of mercury resistance genes but, because of the diversity of genetic determinants, highlight the importance of using multiple detection techniques and gene probes derived from a variety of origins for such studies.     

N-Terminal Domains of Cardiac Myosin Binding Protein C Cooperatively Activate the Thin Filament

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The monocyte-macrophage-mast cell axis in dengue pathogenesis

Dengue virus, the causative agent of dengue disease which may have hemorrhagic complications, poses a global health threat. Among the numerous target cells for dengue virus in humans are monocytes, macrophages and mast cells which are important regulators of vascular integrity and which undergo dramatic cellular responses after infection by dengue virus. The strategic locations of these three cell types, inside blood vessels (monocytes) or outside blood vessels (macrophages and mast cells) allow them to respond to dengue virus infection with the production of both intracellular and secretory factors which affect virus replication, vascular permeability and/or leukocyte extravasation. Moreover, the expression of Fc receptors on the surface of monocytes, macrophages and mast cells makes them important target cells for antibody-enhanced dengue virus infection which is a major risk factor for severe dengue disease, involving hemorrhage. Collectively, these features of monocytes, macrophages and mast cells contribute to both beneficial and harmful responses of importance to understanding and controlling dengue infection and disease.