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A new cluster-based metal–organic framework (MOF) [(Me 2 NH 2 )Cd 3 (OH)(H 2 O) 3 (TATAB) 2 ](DMA) 6 ( 1 , DMA = N , N -dimethylacetamide) with triazine backbones has been successfully prepared using the 4,4′,4″-s-triazin-1,3,5-triyltri- p -aminobenzoic acid (H 3 TATAB) as the organic spaces. The as-prepared 1 was characterized by elemental analysis, powder X-ray diffraction, single-crystal X-ray diffraction and thermogravimetric analysis. The X-ray study result reveals that complex 1 belongs to the tetragonal space group P4 3 2 1 2 and shows a three-dimensional channel-type framework. The luminescent responses of 1 respect to different metal ions were studied, which reveals that 1 shows highly selective and sensitive detection of Hg 2+ via an obvious fluorescence quenching and red-shift of the emission peak. Furthermore, the possible sensing mechanism has also been discussed in this work. [ABSTRACT FROM AUTHOR]

Abstract: Four novel 4-hydroxycoumarin derivatives (4-MBH, 3-MBH, 4-MDT and 3-MDT) were successfully synthesized and their structures were verified by single-crystal X-ray crystallography. All target compounds were evaluated for their in vitro antibacterial activity against Staphylococcus aureus (S. aureus ATCC 29213), methicillin-resistant S. aureus (MRSA XJ 75302), vancomycin-intermediate S. aureus (Mu50 ATCC 700699), and USA 300 (Los Angeles County clone, LAC). The minimum inhibitory concentration and time–kill curves were obtained for the test compounds and antibiotics. Among the tested compounds, 3-MBH showed the most potent antibacterial activities. [Copyright &y& Elsevier]

Phosphorus is one of the most important macronutrients required for plant growth and development. The importance of phosphorylation modification in regulating phosphate (Pi) homeostasis in plants is emerging. We performed phosphoproteomic profiling to characterize proteins whose degree of phosphorylation is altered in response to Pi starvation in rice root. A subset of 554 proteins, including 546 down-phosphorylated and eight up-phosphorylated proteins, exhibited differential phosphorylation in response to Pi starvation. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis with the differentially phosphorylated proteins indicated that RNA processing, transport, splicing and translation and carbon metabolism played critical roles in response to Pi starvation in rice. Levels of phosphorylation of four mitogen-activated protein kinases (MAPKs), including OsMAPK6, five calcium-dependent protein kinases (CDPKs) and OsCK2β3 decreased in response to Pi starvation. The decreased phosphorylation level of OsMAPK6 was confirmed by Western blotting. Mutation of OsMAPK6 led to Pi accumulation under Pi-sufficient conditions. Motif analysis indicated that the putative MAPK, casein kinase 2 (CK2) and CDPK substrates represented about 54.4%, 21.5% and 4.7%, respectively, of the proteins exhibiting differential phosphorylation. Based on the motif analysis, 191, 151 and 46 candidate substrates for MAPK, CK2 and CDPK were identified. These results indicate that modification of phosphorylation profiles provides complementary information on Pi-starvation-induced processes, with CK2, MAPK and CDPK protein kinase families playing key roles in these processes in rice. [ABSTRACT FROM AUTHOR]

Arsenic (As) contamination in agricultural soil can cause phytotoxicity and lead to As accumulation in crops. Rice (Oryza sativa) feeds half of the world's population, but the molecular mechanism of As detoxification is not well understood in rice. In this study, the role of OsNLA1 in arsenate uptake and tolerance in rice was analyzed. OsNLA1 expression was induced in response to As(V) stress. The osnla1 mutant was more sensitive to As(V) stress than those of the wild type (WT). When exposed to As(V), mutation of OsNLA1 resulted in 30% greater As accumulation in roots and shoots of the WT. Although OsPT8 expression was induced after As(V) exposure, the amount of its protein was reduced. Unexpectedly, the osnla1 mutant showed a significant increase in punctate structures of OsPT8-GFP in response to As(V) stress, while the amount of the OsPT8-GFP protein in the osnla1 mutant was greater than in the WT. Combining OsNLA1 mutation with OsPT8 overexpression resulted in As(V) hypersensitivity, As hyperaccumulation, and higher shoot to root ratio of As in rice. These results indicated that OsNLA1 plays an important role in arsenate uptake and tolerance, mainly via regulating the amount of Pi transporters. [ABSTRACT FROM AUTHOR]

Phosphate (Pi), as the main form of phosphorus that can be absorbed by plants, is one of the most limiting macro-nutrients for plants. However, the mechanism for maintaining Pi homeostasis in rice (Oryza sativa) is still not well understood. We identified a P i-starvation- i nduced E 3 ligase (OsPIE1) in rice. Using an in vitro self-ubiquitination assay, we determined the E3 ligase activities of OsPIE1. Using GUS staining and GFP detection, we analyzed tissue expression patterns of OsPIE1 and the subcellular localization of its encoded protein. The function of OsPIE1 in Pi homeostasis was analyzed using OsPIE1 overexpressors and ospie1 mutants. OsPIE1 was localized to the nucleus, and expressed in epidermis, exodermis and sclerenchyma layers of primary root. Under Pi-sufficient condition, overexpression of OsPIE1 upregulated the expression of OsPT2, OsPT3, OsPT10 and OsPAP21b, resulting in Pi accumulation and acid phosphatases (APases) induction in roots. OsSPX2 was strongly suppressed in OsPIE1 overexpressors. Further comparative transcriptome analysis, tissue expression patterns and genetic interaction analysis indicated that the enhancing of Pi accumulation and APase activities upon overexpression of OsPIE1 was (at least in part) caused by repression of OsSPX2. These results indicate that OsPIE1 plays an important role in maintaining Pi homeostasis in rice. [ABSTRACT FROM AUTHOR]

Glioma is the most common neoplasm of the central nervous system (CNS); the progression and outcomes of which are affected by a complicated network of genes and pathways. We chose a gene expression profile of GSE66354 from GEO database to search core biomarkers during the occurrence and development of glioma. A total of 149 samples, involving 136 glioma and 13 normal brain tissues, were enrolled in this article. 1980 differentially expressed genes (DEGs) including 697 upregulated genes and 1283 downregulated genes between glioma patients and healthy individuals were selected using GeoDiver and GEO2R tool. Then, gene ontology (GO) analysis as well as Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were carried out using the Database for Annotation, Visualization and Integrated Discovery (DAVID). Moreover, Cytoscape with Search Tool for the Retrieval of Interacting Genes (STRING) and Molecular Complex Detection (MCODE) plug-in was employed to imagine protein-protein interaction (PPI) of these DEGs. The upregulated genes were enriched in cell cycle, ECM-receptor interaction, and p53 signaling pathway, while the downregulated genes were enriched in retrograde endocannabinoid signaling, glutamatergic synapse, morphine addiction, GABAergic synapse, and calcium signaling pathway. Subsequently, 4 typical modules were discovered by the PPI network utilizing MCODE software. Besides, 15 hub genes were chosen according to the degree of connectivity, including TP53, CDK1, CCNB1, and CCNB2, the Kaplan-Meier analysis of which was further identified. In conclusion, this bioinformatics analysis indicated that DEGs and core genes, such as TP53, might influence the development of glioma, especially in tumor proliferation, which were expected to be promising biomarkers for diagnosis and treatment of glioma. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is a leading cause of disability and mortality in young adults worldwide. The pathophysiology is not fully understood. Programmed necrosis (necroptosis) is a newly identified mechanism of cell death combining features of both apoptosis and necrosis. Receptor-interacting protein 3 (RIP3) plays an important role in programmed necrosis. However, the effect of RIP3-related pathway in TBI is little to be known. We attempted to explore the significance of RIP3 in regulating TBI in vivo. Significantly, TBI induced over-expression of RIP3 in the hippocampus of mice, as well as RIP1 and phosphorylated mixed lineage kinase domain-like protein (MLKL). Mice after TBI exhibited cognitive dysfunction and activation of glia cells, which were significantly attenuated by RIP3-knockout (KO). Moreover, inflammation and oxidative stress in hippocampus were markedly induced by TBI in wild type (WT) mice. Of note, the reduction of pro-inflammatory cytokines and oxidants was observed in RIP3-deficient mice, which was linked to the blockage of NLR pyrin domain containing 3 (NLRP3)/apoptosis-associated speck-like protein containing a CARD (ASC)/Caspase-1 and kelch-like ECH-associated protein 1 (Keap 1) pathways. Further, TBI induced hippocampus apoptosis, evidenced by the increase of cleaved Caspase-8/-3 and poly (ADP)-ribose polymerase (PARP) in WT mice, whereas being decreased by RIP3-knockout. In addition, RIP3 knockout led to phosphorylation of AMP-activated protein kinase α (AMPKα) in hippocampus of mice after TBI. And of note, the in vitro findings indicated that RIP3-ablation attenuated oxidative stress, inflammation and apoptosis in astrocytes, which was dependent on AMPKα activation. Together, suppressing RIP3 might be served as a therapeutic target against brain injury through inhibiting inflammation, oxidative stress and apoptosis. [ABSTRACT FROM AUTHOR]