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阳离子诱导大叶藻叶绿体膜中激发能在PSⅡ和PSⅠ之间分配变化的机理(英文) 总被引:1,自引:0,他引:1
用Ca2+ 和胰酶处理大叶藻(Zostera m arina)叶绿体膜研究了其类囊体膜多肽成分与Mg2+ 诱导其Chla荧光和类囊体膜表面电荷变化之间的相互关系,观察到:1.在正常的叶绿体膜中,Mg2+ 诱导PSⅡ荧光强度的增高与其诱导类囊体膜表面电荷密度的降低密切相关;2.用Ca2+ 处理这种叶绿体膜,除去类囊体膜表面的32~34 kD多肽对Mg2+ 诱导的上述现象无影响;3.如果用胰酶消化Ca2+ 处理过的叶绿体膜,进一步除去膜表面的26 kD多肽,Mg2+诱导的这些现象则全部消失。这些实验结果清楚地表明,在大叶藻的叶绿体膜中,类囊体膜表面的26 kD 多肽是阳离子诱导这两种相关现象的特异性作用部位。对阳离子调节激发能在PSⅡ和PSⅠ之间分配的机理进行了讨论 相似文献
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Wang P Lou PJ Leu S Ouyang P 《Biochemical and biophysical research communications》2002,294(2):448-455
Pre-mRNA splicing occurs in a large macromolecular RNA-protein complex called the spliceosome. The major components of the spliceosome include snRNP and SR proteins. We have previously identified an SR-like protein, pinin (pnn), which is localized not only in nuclear speckles but also at desmosomes. The nuclear localization of pnn is a dynamic process because pnn can be found not only with SR proteins in nuclear speckles but also in enlarged speckles following treatment of cells with RNA polymerase II inhibitors, DRB, and alpha-amanitin. Using adenovirus E1A and chimeric calcitonin/dhfr construct as a splicing reporter minigene in combination with cellular cotransfection, we found that pnn regulates alternative 5(') and 3(') splicing by decreasing the use of distal splice sites. Regulation of 5(') splice site choice was also observed for RNPS1, a general splicing activator that interacts with pnn in nuclear speckles. The regulatory ability of pnn in alternative 5(') splicing, however, was not dependent on RNPS1 and a pnn mutant, lacking the N-terminal 167 amino acids, behaved like a dominant negative species, inhibiting E1A splicing when applied in splicing assays. These results provide direct evidence that pnn functions as a splicing regulator which participates itself directly in splicing reaction or indirectly via other components of splicing machinery. 相似文献
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Ming Ye Qingqing Dai Junbo Zheng Xuesong Jiang Huaiquan Wang Shaofei Lou Kaijiang Yu 《Cell biochemistry and biophysics》2014,70(1):587-591
The purpose of the study is to investigate the effectiveness of serum creatinine, the most common indicator of acute kidney injury (AKI), in predicting the prognosis of critically ill patients after cardiac surgery. Also, we sought to validate the use of this biomarker in assessing the direct outcome of a clinical setting. We selected 592 patients from our hospital; the relevant information including name, disease, gender, age, EuroSCORE, length of stay (LOS), days of mechanical ventilation, days of noninvasive positive pressure ventilation, days of continuous renal replacement treatment, and mortality was recorded. Creatinine of pre-operative, 24, and 48 h post-operation specimens were analyzed. The difference in serum creatinine levels at various time points was compared using t test. Spearman correlation was used to analyze the correlation of serum creatinine to AKI and hard outcomes. Receiver-operating characteristic curves were generated, and the areas under the curves (AUCs) were compared to validate the adequacy of creatinine in predicting the post-operative AKI. The 48 h post-operative and pre-operative serum creatinine were found to be informative in predicting the outcome of patients as indicated by the t test and Spearman correlation analysis. The 48 h creatinine with AUC of 0.811 was indicated to be significantly associated with the hard outcome. However, the 24 h and pre-operative creatinine with AUCs of 0.701 and 0.658, respectively, were not adequately related to the outcomes. In conclusion, contrary to the existing belief that creatinine is not an informative parameter for the diagnosis and prognosis of AKI, we found that when measured at 48 h of cardiac surgery, serum creatinine is reflective of the outcome. 相似文献
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Examination of the Kinetics of Herpes Simplex Virus Glycoprotein D Binding to the Herpesvirus Entry Mediator, Using Surface Plasmon Resonance 总被引:4,自引:8,他引:4
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Sharon H. Willis Ann H. Rux Charline Peng J. Charles Whitbeck Anthony V. Nicola Huan Lou Wangfang Hou Lisa Salvador Roselyn J. Eisenberg Gary H. Cohen 《Journal of virology》1998,72(7):5937-5947
Previously, we showed that truncated soluble forms of herpes simplex virus (HSV) glycoprotein D (gDt) bound directly to a truncated soluble form of the herpesvirus entry mediator (HveAt, formerly HVEMt), a cellular receptor for HSV. The purpose of the present study was to determine the affinity of gDt for HveAt by surface plasmon resonance and to compare and contrast the kinetics of an expanded panel of gDt variants in binding to HveAt in an effort to better understand the mechanism of receptor binding and virus entry. Both HveAt and gDt are dimers in solution and interact with a 2:1 stoichiometry. With HveAt, gD1(306t) (from the KOS strain of HSV-1) had a dissociation constant (KD) of 3.2 × 10−6 M and gD2(306t) had a KD of 1.5 × 10−6 M. The interaction between gDt and HveAt fits a 1:1 Langmuir binding model, i.e., two dimers of HveAt may act as one binding unit to interact with one dimer of gDt as the second binding unit. A gD variant lacking all signals for N-linked oligosaccharides had an affinity for HveAt similar to that of gD1(306t). A variant lacking the bond from cysteine 1 to cysteine 5 had an affinity for HveAt that did not differ from that of the wild type. However, variants with double cysteine mutations that eliminated either of the other two disulfide bonds showed decreased affinity for HveAt. This result suggests that two of the three disulfide bonds of gD are important for receptor binding. Four nonfunctional gDt variants, each representing one functional domain of gD, were also studied. Mutations in functional regions I and II drastically decreased the affinity of gDt for HveAt. Surprisingly, a variant with an insertion in functional region III had a wild-type level of affinity for HveAt, suggesting that this domain may function in virus entry at a step other than receptor binding. A variant with a deletion in functional region IV [gD1(Δ290-299t)] exhibited a 100-fold enhancement in affinity for HveAt (KD = 3.3 × 10−8 M) due mainly to a 40-fold increase in its kinetic on rate. This agrees with the results of other studies showing the enhanced ability of gD1(Δ290-299t) to block infection. Interestingly, all the variants with decreased affinities for HveAt exhibited decreased kinetic on rates but only minor changes in their kinetic off rates. The results suggest that once the complex between gDt and HveAt forms, its stability is unaffected by a variety of changes in gD. 相似文献
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新疆地震断裂带次生植物根际土壤微生物碳源利用 总被引:5,自引:0,他引:5
利用BIOLOG技术研究了新疆富蕴地震断裂带6种次生植物对根际土壤微生物碳源利用的影响.结果表明:多数植物根际土壤养分显著高于对照.6种根际土壤的平均颜色变化率差异显著,且均高于对照.次生植物不影响根际土壤微生物碳源利用的丰富度,但改变了其优势度和均匀度.不同处理根际土壤微生物碳源利用存在差异,主要体现在对糖类、氨基酸类、羧酸类的利用上.断裂带上次生植物的出现使土壤微生物利用碳源的类型由酚类向糖类、羧酸类转变.土壤速效钾含量与土壤微生物对聚合物(r=-0.84)、胺类(r=-0.83)的利用呈负相关.新疆地震断裂带的次生植物能显著增强土壤微生物的碳源利用能力,改变碳源利用类型.密刺蔷薇和蓍在提高土壤微生物碳源利用能力和改善土壤养分方面效果最佳. 相似文献
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Simsek D Brunet E Wong SY Katyal S Gao Y McKinnon PJ Lou J Zhang L Li J Rebar EJ Gregory PD Holmes MC Jasin M 《PLoS genetics》2011,7(6):e1002080
Nonhomologous end-joining (NHEJ) is the primary DNA repair pathway thought to underlie chromosomal translocations and other genomic rearrangements in somatic cells. The canonical NHEJ pathway, including DNA ligase IV (Lig4), suppresses genomic instability and chromosomal translocations, leading to the notion that a poorly defined, alternative NHEJ (alt-NHEJ) pathway generates these rearrangements. Here, we investigate the DNA ligase requirement of chromosomal translocation formation in mouse cells. Mammals have two other DNA ligases, Lig1 and Lig3, in addition to Lig4. As deletion of Lig3 results in cellular lethality due to its requirement in mitochondria, we used recently developed cell lines deficient in nuclear Lig3 but rescued for mitochondrial DNA ligase activity. Further, zinc finger endonucleases were used to generate DNA breaks at endogenous loci to induce translocations. Unlike with Lig4 deficiency, which causes an increase in translocation frequency, translocations are reduced in frequency in the absence of Lig3. Residual translocations in Lig3-deficient cells do not show a bias toward use of pre-existing microhomology at the breakpoint junctions, unlike either wild-type or Lig4-deficient cells, consistent with the notion that alt-NHEJ is impaired with Lig3 loss. By contrast, Lig1 depletion in otherwise wild-type cells does not reduce translocations or affect microhomology use. However, translocations are further reduced in Lig3-deficient cells upon Lig1 knockdown, suggesting the existence of two alt-NHEJ pathways, one that is biased toward microhomology use and requires Lig3 and a back-up pathway which does not depend on microhomology and utilizes Lig1. 相似文献