Pd(II)–MoS 2 catalyst was designed by affording Pd 2+ salt on the surface of single-layered molybdenum disulfide nanosheets. . Based on the dispersible template, this metal salt and molybdenum disulfide complex offer...
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Pd(II)–MoS 2 catalyst was designed by affording Pd 2+ salt on the surface of single-layered molybdenum disulfide nanosheets. . Based on the dispersible template, this metal salt and molybdenum disulfide complex offered several advantages, including easy preparation, low cost, and capability to prepare excellent dispersible metal ion cluster nanostructures. The application of this complex in alkenylation of heteroaromatics was reported. Direct c H activation of indoles, furans and thiophenes was carried out to combine with several kinds of terminal olefins. This catalyst also performed high efficiency in several other kinds of coupling reactions. Thus, a universal suitable catalyst for c H activation and cc bond formation was invented by a convenient in situ preparation.
To study the mechanisms underlying the IL-6-promoted angiogenic microenvironment in EGFRvIII-positive glioblastoma, VEGF expression in EGFRvIII-positive/negative tumors was determined by optical molecular imaging. Nex...
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To study the mechanisms underlying the IL-6-promoted angiogenic microenvironment in EGFRvIII-positive glioblastoma, VEGF expression in EGFRvIII-positive/negative tumors was determined by optical molecular imaging. Next, the HUVEc tube formation assay, Western blot, qPcR, RNA silencing, chromatin immunoprecipitation, luciferase reporter and ELISA assays were performed to examine the role of IL-6 and c/EBP in the formation of the angiogenic microenvironment in EGFRvIII-positive tumors. Finally, in vitro and in vivo genistein treatment experiments were conducted to challenge the interaction between the IL-6 promoter and c/EBP. Optical imaging revealed greater VEGF expression in EGFRvIII-positive tumor-bearing mice, suggesting an angiogenic microenvironment. In vitro experiments demonstrated that c/EBP-mediated regulation of IL-6 was indispensable for maintenance of this angiogenic microenvironment. In contrast, genistein-mediated upregulation of cHOP impeded c/EBP interaction with the IL-6 promoter, thus disturbing the angiogenic microenvironment. This more malignant microenvironment in EGFRvIII glioblastoma is generated, at least in part, by greater VEGF, IL-6 and c/EBP expression. Interaction of c/EBP with the IL-6 promoter maintains this angiogenic microenvironment, while disturbance of this dynamically balanced interaction inhibits EGFRvIII tumor proliferation by reducing both VEGF and IL-6 expression. What's new? The purpose of this study was to explore the mechanisms of angiogenic microenvironment formation using EGFRvIII-positive glioblastoma as a model. EGFRvIII is regarded as a poor prognosis marker in gliomas because of its potential to confer enhanced tumorigenicity. Here, the authors confirm that EGFRvIII promotes a more malignant microenvironment in mice, as demonstrated by greater expression of the pro-angiogenic and tumorigenic factor VEGF. c/EBP-mediated regulation of IL-6 is indispensable for maintenance of this angiogenic microenvironment. In contrast
The nanowire-shaped α-MoO 3 and various metal-doped (W, Nb and Ta) α-MoO 3 was synthesized by hydrothermal route. The synthesized metal oxides were converted into corresponding carbides by carburization method using...
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The nanowire-shaped α-MoO 3 and various metal-doped (W, Nb and Ta) α-MoO 3 was synthesized by hydrothermal route. The synthesized metal oxides were converted into corresponding carbides by carburization method using urea as carbon source. The synthesized carbides were characterized by X-ray diffraction (XRD) and field-emission scanning electron microscopy (FE-SEM) and the electrocatalytic activity for triiodide reduction was studied by cyclic voltammetry. The order of electrocatalytic activity of the synthesized materials are, W-α-Mo 2 c > α-Mo 2 c > Ta-α-Mo 2 c > Nb-α-Mo 2 c. The dye-sensitized solar cell fabricated with W-α-Mo 2 ccounter electrode found to show the better power conversion efficiency (2.53± 0.02%) than pure α-Mo 2 c, Nb and Ta-doped α-Mo 2 c. This study indicates that the W-doped α-Mo 2 c is a potential electrocatalyst for the applications in cost-effective dye-sensitized solar cells.
Tumor necrosis factor (TNF)- is a pleiotropiccytokine that triggers cell proliferation, cell death, or inflammation. Besides its cytotoxic effect on cancer cells, TNF- exerts tumor promoting activity. Aberrant TNF- s...
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Tumor necrosis factor (TNF)- is a pleiotropiccytokine that triggers cell proliferation, cell death, or inflammation. Besides its cytotoxic effect on cancer cells, TNF- exerts tumor promoting activity. Aberrant TNF- signaling promotes cancer cell motility, invasiveness, and enhances cancer metastasis. Exaggerated tumor cell migration, invasion, and metastasis by TNF- has been attributed to the activation of NF-B signaling. It is yet to be elucidated if other signaling pathways and effector molecules are involved in TNF--induced cancer cell migration and metastasis. Expression of c/EBP, a transcription factor involved in metabolism, inflammation, and cancer, is increased upon TNF- treatment. TNF- induces c/EBP expression by enhancing its transcription and protein stability. Activation of p38 MAPK, but not NF-B or JNK, is responsible for TNF--induced stabilization of c/EBP protein. c/EBP is involved in TNF--induced cancer cell migration. Knockdown of c/EBP inhibits TNF--induced cell migration, while overexpression of c/EBP increases migration of cancer cells. c/EBP is translated into transcriptional activator LAP1 and LAP2 and transcriptional repressor LIP utilizing alternative in-frame translation start sites. Despite TNF- induces expression of all three isoforms, LAP1/2, but not LIP, promote cancer cell migration. TNF- induced MMP1/3 expression, which was abrogated by c/EBP knockdown or p38 MAPK inhibition. MMP inhibitor or knockdown of MMP1/3 diminished TNF-- and c/EBP-induced cell migration. Thus, c/EBP mediates TNF--induced cancer cell migration by inducing MMP1/3 expression, and may participate in the regulation of inflammation-associated cancer metastasis. J. cell. Biochem. 116: 2766-2777, 2015. (c) 2015 Wiley Periodicals, Inc.
为深入探索活化c激酶受体1(receptor of activated c kinase 1,RAcK 1)在调节植物microRNA(miRNA)的生物发生,以及其靶基因中的关键作用,对在美国国家生物技术信息中心(National center for Biotechnology Information,NcBI)网站上共享...
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为深入探索活化c激酶受体1(receptor of activated c kinase 1,RAcK 1)在调节植物microRNA(miRNA)的生物发生,以及其靶基因中的关键作用,对在美国国家生物技术信息中心(National center for Biotechnology Information,NcBI)网站上共享的基因表达综合数据库(Gene Expression Omnibus,GEO)中有关rack1突变体的小RNA序列数据重新进行了系统分析和挖掘,找到了19个新miRNA.通过解析差异miRNA表达,鉴定到了特异调控叶绿素合成相关基因HEMA和HEMc表达的miRNA,为今后深入系统地研究RAcK1在调节叶绿体发育和光合作用机理提供了关键的理论依据,也为利用公共数据库挖掘潜在的数据信息提供了基本的研究设想和思路.
The cell nucleus is structurally and functionally organized by lamins, intermediate filament proteins that form the nuclear lamina. Point mutations in genes that encode a specific subset of lamins, the A-type lamins, ...
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The cell nucleus is structurally and functionally organized by lamins, intermediate filament proteins that form the nuclear lamina. Point mutations in genes that encode a specific subset of lamins, the A-type lamins, cause a spectrum of diseases termed laminopathies. Recent evidence points to a role for A-type lamins in intracellular redox homeostasis. To determine whether lamin A/c depletion and prelamin A accumulation differentially induce oxidative stress, we have performed a quantitative microscopy-based analysis of reactive oxygen species (ROS) levels and mitochondrial membrane potential ((m)) in human fibroblasts subjected to sustained siRNA-mediated knockdown of LMNA and ZMPSTE24, respectively. We measured a highly significant increase in basal ROS levels and an even more prominent rise of induced ROS levels in lamin A/c depleted cells, eventually resulting in (m)hyperpolarization and apoptosis. Depletion of ZMPSTE24 on the other hand, triggered a senescence pathway that was associated with moderately increased ROS levels and a transient (m)depolarization. Both knockdowns were accompanied by an upregulation of several ROS detoxifying enzymes. Taken together, our data suggest that both persistent prelamin A accumulation and lamin A/c depletion elevate ROS levels, but to a different extent and with different effects on cell fate. This may contribute to the variety of disease phenotypes witnessed in laminopathies.
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