EVIDENCE FOR SPECIES ' DIFFERENCES IN TIlE EFFECT OF SERUM 7-GLOBULIN CONCENTRATION ON

The serum y-globulin level depends on a dynamic equilibrium between synthesis and catabolism. The mechanisms which regulate this equilibrium are not well understood, but a balance must exist between the rate of production and the rate of breakdown in order to maintain a constant serum-/-globulin concentration. Injections of exogenous y-globulin into mice increase the rate of catabolism of isotopically labeled homologous (mouse) y-globulin (1). The rate of catabolism of homologous y-globulin is also more rapid in hyperimmunized mice (1) or mice harboring y-globulin-producing plasma cell tumors (2). On the other hand, germfree mice, which have subnormal serum y-globulin concentrations, have slower rates of y-globulin breakdown than normal mice (3). The rate of T-globulin catabolism also appears to be related to the serum y-globulin concentration in man (4-10). In guinea pigs, however, the rates of homologous y-globulin catabolism are the same in germfree and normal animals in spite of up to 6-fold differences in the serum ")'-globulin levels (11), suggesting that the fractional catabolic rate of homologous y-globulin is independent of the serum level in these animals

Identification and Functional Characterization of CbaR, a MarR-Like Modulator of the cbaABC-Encoded

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sn-Glycerol-1-Phosphate-Forming Activities in Archaea: Separation of Archaeal Phospholipid Biosynthesis and

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ORIGINAL ARTICLE Adiponectin Reduces Plasma Triglyceride by Increasing

OBJECTIVE—Adiponectin is an adipocyte-derived hormone that plays an important role in glucose and lipid metabolism. The main aims of this study are to investigate the effects of adiponectin on VLDL triglyceride (VLDL-TG) metabolism and the underlying mechanism. RESEARCH DESIGN AND METHODS—Adenoviruses were used to generate a mouse model with elevated circulating adiponectin. HepG2 and C2C12 cells were treated with recombinant human adiponectin. RESULTS—Three days after Ad-mACRP30 adenovirus injection, plasma adiponectin protein levels were increased 12-fold. All three main multimeric adiponectin molecules were proportionally elevated. Fasting plasma TG levels were significantly decreased (�40%) in the mice with elevated adiponectin in circulation, as were the plasma levels of large and medium VLDL subclasses. Although apolipoprotein B mRNA levels were robustly suppressed in the livers of adiponectin-overexpressing mice and in cultured HepG2 cells treated with recombinant human adiponectin, hepatic VLDL-TG secretion rates were not altered by elevated plasma adiponectin. However, Ad-mACRP30–treated mice exhibited a significant increase of postheparin plasma lipoprotein lipase (LPL) activity compared with mice that received control viral vector. Skeletal muscle LPL activity and mRNA levels of LPL and VLDL receptor (VLDLr) were also increased in Ad-mACRP30– treated mice. Recombinant human adiponectin treatment increased LPL and VLDLr mRNA levels in differentiated C1C12 myotubes. CONCLUSIONS—These results suggest that adiponectin decreases plasma TG levels by increasing skeletal muscle LPL and VLDLr expression and consequently VLDL-TG catabolism

: Cloning, Characterization, and Expression of the

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The phn Genes of Burkholderia sp. Strain RP007 Constitute a Divergent Gene Cluster for Polycyclic Aromatic

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Involvement of the Cra Global Regulatory Protein in the Expression of the iscRSUA Operon, Revealed during Studies of Tricarballylate

In Salmonella enterica, tricarballylate (Tcb) catabolism requires function of TcuB, a membrane-bound protein that contains [4Fe-4S] clusters and heme. TcuB transfers electrons from reduced flavin adenine dinucleotide in the Tcb dehydrogenase (TcuA) to electron acceptors in the membrane. We recently showed that functions needed to assemble [Fe-S] clusters (i.e., the iscRSUA-hscBA-fdx operon) compensate for the lack of ApbC during growth of an apbC strain on Tcb. ApbC had been linked to [Fe-S] cluster metabolism, and we showed that an apbC strain had decreased TcuB activity. Here we report findings that expand our understanding of the regulation of expression of the iscRSUA genes in Salmonella enterica. We investigated why low levels of glucose or other saccharides restored growth of an apbC strain on Tcb. Here we report the following findings. (i) A <1 mM concentration of glucose, fructose, ribose, or glycerol restores growth of an apbC strain on Tcb. (ii) The saccharide effect results in increased levels of TcuB activity. (iii) The saccharide effect depends on the global regulatory protein Cra. (iv) Putative Cra binding sites are present in the regulatory region of the iscRSUA operon. (v) Cra protein binds to all three sites in the iscRSUA promoter region in a concentrationdependent fashion. To our knowledge, this is the first report of the involvement of Cra in [Fe-S] cluster assembly. Tricarballylate (Tcb) is a citrate analog that causes gras

Inhibition of T Cell Proliferation by Macrophage

We have recently shown that expression of the enzyme indoleamine 2,3-dioxygenase (IDO) during murine pregnancy is required to prevent rejection of the allogeneic fetus by maternal T cells. In addition to their role in pregnancy, IDO-expressing cells are widely distributed in primary and secondary lymphoid organs. Here we show that monocytes that have differentiated under the influence of macrophage colony-stimulating factor acquire the ability to suppress T cell proliferation in vitro via rapid and selective degradation of tryptophan by IDO. IDO was induced in macrophages by a synergistic combination of the T cell–derived signals IFN- � and CD40ligand. Inhibition of IDO with the 1-methyl analogue of tryptophan prevented macrophagemediated suppression. Purified T cells activated under tryptophan-deficient conditions were able to synthesize protein, enter the cell cycle, and progress normally through the initial stages of G1, including upregulation of IL-2 receptor and synthesis of IL-2. However, in the absence of tryptophan, cell cycle progression halted at a mid-G1 arrest point. Restoration of tryptophan to arrested cells was not sufficient to allow further cell cycle progression nor was costimulation via CD28. T cells could exit the arrested state only if a second round of T cell receptor signaling was provided in the presence of tryptophan. These data reveal a novel mechanism by whic

Gene Structure, Organization, Expression, and Potential Regulatory Mechanisms of Arginine Catabolism in Enterococcus faecalis

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A Genetic Locus Necessary for Rhamnose Uptake and Catabolism in Rhizobium leguminosarum bv. trifolii

Rhizobium leguminosarum bv. trifolii mutants unable to catabolize the methyl-pentose rhamnose are unable to compete effectively for nodule occupancy. In this work we show that the locus responsible for the transport and catabolism of rhamnose spans 10,959 bp. Mutations in this region were generated by transposon mutagenesis, and representative mutants were characterized. The locus contains genes coding for an ABC-type transporter, a putative dehydrogenase, a probable isomerase, and a sugar kinase necessary for the transport and subsequent catabolism of rhamnose. The regulation of these genes, which are inducible by rhamnose, is carried out in part by a DeoR-type negative regulator (RhaR) that is encoded within the same transcript as the ABC-type transporter but is separated from the structural genes encoding the transporter by a terminator-like sequence. RNA dot blot analysis demonstrated that this terminator-like sequence is correlated with transcript attenuation only under noninducing conditions. Transport assays utilizing tritiated rhamnose demonstrated that uptake of rhamnose was inducible and dependent upon the presence of the ABC transporter at this locus. Phenotypic analyses of representative mutants from this locus provide genetic evidence that the catabolism of rhamnose differs from previously described methyl-pentose catabolic pathways