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991.
992.
993.
994.
Identification of shiga toxin-producing bacteria by a new immuno-capture toxin gene PCR 总被引:4,自引:0,他引:4
Mechanisms and occurrence of macrolide resistance in the periodontal pathogen Treponema denticola have received little attention. In this study, erythromycin resistance due to mutations in the genes encoding T. denticola 23S rRNA was investigated. The T. denticola genome was shown to contain two copies of 23S rDNA. 23S rRNA genes of nine erythromycin-resistant isolates derived from T. denticola were amplified and sequences were analyzed. All the erythromycin-resistant strains had at least one A-->G transition mutation at the 23S rRNA gene sequence cognate to position A2058 in Escherichia coli 23S rDNA. This suggests that antibiotic pressure is sufficient to select for point mutations that confer resistance in this organism. 相似文献
995.
Binding of ouabain to Na(+)/K(+)-ATPase activates tyrosine phosphorylation of the epidermal growth factor receptor (EGFR), Src, and p42/44 mitogen-activated protein kinases (MAPKs) in both cardiac myocytes and A7r5 cells. Here, we explored the roles of Src and the EGFR in the ouabain-invoked pathways that lead to the activation of MAPKs. Exposure of A7r5 and LLC-PK1 cells to ouabain caused a dose-dependent inhibition of Na(+)/K(+)-ATPase activity, which correlated well with ouabain-induced activation of Src and MAPKs in these cells. Immunoprecipitation experiments showed that ouabain stimulated Src binding to Na(+)/K(+)-ATPase in a dose- and time-dependent manner and increased phosphorylation of Src at Tyr(418) but had no effect on Tyr(529) phosphorylation. Ouabain failed to activate MAPKs in A7r5 cells that were pretreated with the Src inhibitor PP2 and in SYF cells in which Src family kinases are knocked out. Preincubation with AG1478, but not AG1295, also blocked the effects of ouabain on p42/44 MAPKs in A7r5 cells. Significantly, both herbimycin A and PP2 abrogated ouabain-induced but not epidermal growth factor-induced Src binding to the EGFR and the subsequent EGFR tyrosine phosphorylation. Ouabain also failed to affect tyrosine phosphorylation of the EGFR in SYF cells. In addition, unlike epidermal growth factor, ouabain did not increase EGFR autophosphorylation at Tyr(1173). These findings clearly indicate that ouabain transactivates the EGFR by activation of Src and stimulation of Src binding to the EGFR. Furthermore, we found that the transactivated EGFR was capable of recruiting and phosphorylating the adaptor protein Shc. This resulted in increased binding of another adaptor protein Grb2 to the Src-EGFR complex and the subsequent activation of Ras and MAPKs. Taken together, these new findings suggest that Src mediates the inter-receptor cross-talk between Na(+)/K(+)-ATPase and the EGFR to transduce the signals from ouabain to the Ras/MAPK cascade. 相似文献
996.
We compared photoinhibition sensitivity to high irradiance (HI) in wild-type barley (wt) and both its chlorina f
104-nuclear gene mutant, that restricts chlorophyll (Chl) a and Chl b synthesis, and its f
2-nuclear gene mutant, that inhibits all Chl b synthesis. Both Fv/Fm and PS2 decreased more significantly in f
2 than f
104 and wt with duration of HI exposure. Chl degraded more rapidly in the f
2 than in either f
104 or wt. Most sensitivity to photoinhibition was exhibited for f
2, whereas there was little difference in response to HI between the f
104 and wt. The highest de-epoxidation (DES) value at every time point of exposure to HI was measured for f
2, whereas the wt had the lowest value among the three strains. There were two lifetime components resolved for the conversion of violaxanthin (V) to zeaxanthin plus antheraxanthin (Z + A). The most rapid lifetime was around 6 min and the slower lifetime was >140 min, in both the mutants and wt. However, the wt and f
104 both displayed larger amplitudes of both de-epoxidation lifetimes than f
2. The difference between the final de-epoxidation state (DES = [Z + A]/[V + A + Z]) in the light compared to the dark expressed as DES for wt, f
104, and f
2 was 0.630, 0.623, and 0.420, respectively. The slow lifetime component and overall larger DES in the wt and f
104 correlated with more photoprotection, as indicated by relatively higher Fv/Fm and PS2, compared to the f
2. Hence the photoprotection against photoinhibition has no relationship with the absolute DES value, but there is a strong relationship with de-epoxidation rate and relative extent or DES. 相似文献
997.
998.
Meng Xie Guodong Ren Chi Zhang Bin Yu 《The Plant journal : for cell and molecular biology》2012,72(3):491-500
Studies have identified a sub‐group of SGS3‐LIKE proteins including FDM1–5 and IDN2 as key components of RNA‐directed DNA methylation pathway (RdDM). Although FDM1 and IDN2 bind RNAs with 5′ overhangs, their functions in the RdDM pathway remain to be examined. Here we show that FDM1 interacts with itself and with IDN2. Gel filtration suggests that FDM1 may exist as a homodimer in a heterotetramer complex in vivo. The XH domain of FDM1 mediates the FDM1–FDM1 and FDM1–IDN2 interactions. Deletion of the XH domain disrupts FDM1 complex formation and results in loss‐of‐function of FDM1. These results demonstrate that XH domain‐mediated complex formation of FDM1 is required for its function in RdDM. In addition, FDM1 binds unmethylated but not methylated DNAs through its coiled‐coil domain. RNAs with 5′ overhangs does not compete with DNA for binding by FDM1, indicating that FDM1 may bind DNA and RNA simultaneously. These results provide insight into how FDM1 functions in RdDM. 相似文献
999.
Kelly M. Clapp Hwei-Ming Peng Gary J. Jenkins Michael J. Ford Yoshihiro Morishima Miranda Lau Yoichi Osawa 《The Journal of biological chemistry》2012,287(51):42601-42610
Nitric-oxide synthase, a cytochrome P450-like hemoprotein enzyme, catalyzes the synthesis of nitric oxide, a critical signaling molecule in a variety of physiological processes. Our laboratory has discovered that certain drugs suicide-inactivate neuronal nitric-oxide synthase (nNOS) and lead to the preferential ubiquitination of the inactivated nNOS by an Hsp70- and CHIP (C terminus of Hsc70-interacting protein)-dependent process. To further understand the process by which altered nNOS is recognized, ubiquitinated, and proteasomally degraded, we examined the sites of ubiquitination on nNOS. We utilized an in vitro ubiquitination system containing purified E1, E2 (UbcH5a), Hsp70, and CHIP that recapitulates the ability of the cells to selectively recognize and ubiquitinate the altered forms of nNOS. LC-MS/MS analysis of the tryptic peptides obtained from the in vitro ubiquitinated nNOS identified 12 ubiquitination sites. Nine of the sites were within the oxygenase domain and two were in the calmodulin-binding site, which links the oxygenase and reductase domains, and one site was in the reductase domain. Mutational analysis of the lysines in the calmodulin-binding site revealed that Lys-739 is a major site for poly-ubiquitination of nNOS in vitro and regulates, in large part, the CHIP-dependent degradation of nNOS in HEK293 cells, as well as in in vitro studies with fraction II. Elucidating the exact site of ubiquitination is an important step in understanding how chaperones recognize and trigger degradation of nNOS. 相似文献
1000.
Ping Xie WeiWei Zhang Songtao Yuan Zhiqiang Chen Qin Yang DongQing Yuan Feng Wang QingHuai Liu 《PloS one》2012,7(12)