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The rnf genes in Rhodobacter capsulatus are essential for nitrogen fixation in the light. Because R. capsulatus grows readily on N2 in the dark by anaerobic respiration with dimethylsulfoxide, the diazotrophic capacities of various strains in the dark were
examined. No rnf mutants tested grew diazotrophically, and a nonpolar fdxN-null mutant showed decreased diazotrophic growth in the dark, suggesting that the Rnf and FdxN proteins form the primary
electron donor pathway to nitrogenase in the dark as well as in the light. Nonphotosynthetic mutants lacking the component
of cyclic electron transport grew diazotrophically and the levels of Rnf proteins were similar to those of the wild-type.
These results indicate that rnf gene products play an essential role in nitrogen fixation without any functional link to the cyclic electron transport system.
Received: 19 August 1997 / Accepted: 20 January 1998 相似文献
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Hirotaka Kashiwagi Masateru Ohta Yoshiyuki Ono Kenji Morikami Susumu Itoh Hideki Sato Tadakatsu Takahashi 《Bioorganic & medicinal chemistry》2013,21(3):712-721
From our research of nonsecosteroidal vitamin D3 derivatives with gamma hydroxy carboxylic acid, we identified compound 6, with two CF3 groups in the side chain, as a most potent vitamin D receptor (VDR) agonist that shows superagonistic activity in VDRE reporter gene assay, MG-63 osteocalcin production assay and HL-60 cell differentiation assay. Compound 6 demonstrated that fluorination is as effective in the case of our nonsecosteroidal scaffold as in the case of secosteroidal VD3 analogs. X-ray analysis of the VDR with compound 6 revealed all of the six fluorine atoms of the hexafluoropropanol (HFP) moiety in the side chain effectively interacting with the VDR by both steric (van der Waals) and electrostatic (hydrogen bond, NH–F and CH–F) interactions. The HFP moiety of 6 effectively interacts with helix 12 (H12) of the VDR and stabilizes the position and the orientation of H12, which could result in stabilizing the coactivator and enhancing the VDR agonistic activity. 相似文献
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Hirotaka Matsuo Tappei Takada Akiyoshi Nakayama Toru Shimizu Masayuki Sakiyama Seiko Shimizu 《Nucleosides, nucleotides & nucleic acids》2014,33(4-6):266-274
ATP-binding cassette transporter, sub-family G, member 2 (ABCG2/BCRP) is identified as a high-capacity urate exporter, and its dysfunction has an association with serum uric acid levels and gout/hyperuricemia risk. Generally, hyperuricemia has been classified into urate “overproduction type,” “underexcretion type,” and “combined type” based on only renal urate excretion, without considering an extra-renal pathway such as gut excretion. In this study, we investigated the effects of ABCG2 dysfunction on human urate handling and the mechanism of hyperuricemia.Clinical parameters for urate handling including urinary urate excretion (UUE) were examined in 644 Japanese male outpatients with hyperuricemia. The severity of their ABCG2 dysfunction was estimated by genotype combination of two common ABCG2 variants, nonfunctional Q126X (rs72552713) and half-functional Q141K (rs2231142).Contrary to the general understanding that ABCG2 dysfunction leads to decreased renal urate excretion, UUE was significantly increased by ABCG2 dysfunction (P = 3.60 × 10?10). Mild, moderate, and severe ABCG2 dysfunctions significantly raised the risk of “overproduction” hyperuricemia including overproduction type and combined type, conferring risk ratios of 1.36, 1.66, and 2.35, respectively.The present results suggest that common dysfunctional variants of ABCG2 decrease extra-renal urate excretion including gut excretion and cause hyperuricemia. Thus, “overproduction type” in the current concept of hyperuricemia should be renamed “renal overload type,” which is caused by two different mechanisms, “extra-renal urate underexcretion” and genuine “urate overproduction.”Our new concept will lead to a more accurate diagnosis and more effective therapeutic strategy for hyperuricemia and gout. 相似文献
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