Biological Trace Element Research - The purpose of this study was to evaluate the protective effect of Du-Zhong cortex extract (DZCE) on lead acetate-induced bone loss in rats. Forty female... 相似文献
BcMAF2plays a key role in flowering regulation by controllingBcTEM1, BcSOC1andBCSPL15in
Pak-choi.
Abstract
Flowering is a key event in the life cycle of plants. Flowering time shows an extensive variation from different Pak-choi (Brassica rapa ssp. chinensis) cultivars. However, the regulation mechanism of flowering in Pak-choi remains rarely known. In this study, a systematic identification and functional analysis of a Pak-choi MADS Affecting Flowering (MAF) gene, BcMAF2, was carried out. BcMAF2 encoded a protein containing a conserved MADS-box domain, which was localized in the nucleus. QPCR analysis indicated that the expression of BcMAF2 was higher in the leaves and flowers. Overexpression of BcMAF2 in Arabidopsis showed that BcMAF2 repressed flowering, which was further confirmed by silencing endogenous BcMAF2 in Pak-choi. In addition, Tempranillo 1 (TEM1) expression was up-regulated and MAF2 expression was down-regulated in the BcMAF2-overexpressing Arabidopsis. The expression of BcMAF2 and BcTEM1 was down-regulated in BcMAF2-silencing Pak-choi plants. The yeast one-hybrid, dual luciferase and qPCR results revealed that BcMAF2 protein could directly bind to BcTEM1 promoter and activate its expression, which was not reported in Arabidopsis. Meanwhile, a self-inhibition was found in BcMAF2. Taken together, this work suggested that BcMAF2 could repress flowering by directly activating BcTEM1.
Photosynthesis Research - Crassulacean acid metabolism (CAM) is a specialized photosynthetic pathway present in a variety of genera including many epiphytic orchids. CAM is under circadian control... 相似文献
Molecular Biology Reports - The complete genome sequence provides the opportunity for genome-wide and coding region analysis of SSRs in the king cobra and for cross-species identification of... 相似文献
Single nucleotide polymorphism (SNP) interactions can explain the missing heritability of common complex diseases. Many interaction detection methods have been proposed in genome-wide association studies, and they can be divided into two types: population-based and family-based. Compared with population-based methods, family-based methods are robust vs. population stratification. Several family-based methods have been proposed, among which Multifactor Dimensionality Reduction (MDR)-based methods are popular and powerful. However, current MDR-based methods suffer from heavy computational burden. Furthermore, they do not allow for main effect adjustment. In this work we develop a two-stage model-based MDR approach (TrioMDR) to detect multi-locus interaction in trio families (i.e., two parents and one affected child). TrioMDR combines the MDR framework with logistic regression models to check interactions, so TrioMDR can adjust main effects. In addition, unlike consuming permutation procedures used in traditional MDR-based methods, TrioMDR utilizes a simple semi-parameter P-values correction procedure to control type I error rate, this procedure only uses a few permutations to achieve the significance of a multi-locus model and significantly speeds up TrioMDR. We performed extensive experiments on simulated data to compare the type I error and power of TrioMDR under different scenarios. The results demonstrate that TrioMDR is fast and more powerful in general than some recently proposed methods for interaction detection in trios. The R codes of TrioMDR are available at: https://github.com/TrioMDR/TrioMDR. 相似文献
Abnormal expression of tumour necrosis factor-α (TNF-α) can lead to various pathological reactions, such as arthritis, psoriasis, krone disease, etc. p38 mitogen-activated protein kinase (p38 MAPK) is an important signal transduction enzyme that plays important roles in influencing the release of intracellular TNF-α factor. It is very meaningful to study the targeting kinase with specific inhibitors in the treatment of related diseases. In order to achieve a deeper insight, it is necessary to analyse the structural characteristics and the action mode of the p38 MAPK inhibitors in the active site. In the study, a ligand-based common feature pharmacophore model and the receptor structure-based pharmacophore model were constructed, respectively. Their common chemical features consisted of the hydrophobic groups (H) and the hydrogen bond acceptors (A), and kept the consistency of spatial structure distribution. Then, the molecular docking and molecular dynamics simulation were performed with the eight training set compounds. The binding characteristics of molecules binding were described in the topological region of the active site. Finally, the structure–activity relationship (SAR) was obtained by analysing docking results with the different pharmacophore models. This research leads to the proposal of an interaction model in the p38 MAPK active site and provides guidance for the screening and design of more potent and selective p38 MAPK inhibitors. 相似文献
Diabetes induced a serious of complications including diabetic retinopathy. Our study aimed to investigate the role of Stromal cell-derived factor 1 (SDF-1) and its receptor CXCR4 in diabetic retinopathy. A mice model of diabetic retinopathy was established, and expression of SDF-1 and CXCR4 in retina was examined by Real-time quantitative PCR (qRT-PCR). Cells of human retinal pigment epithelial cell line ARPE-19 were treated with CXCR4 siRNAs and expression vector, and cell viability was detected by MTT assay. We found that expression of SDF-1 and CXCR4 in retina was significantly downregulated in mice with diabetic retinopathy than in normal healthy mice. High glucose treatment downregulated the expression of SDF-1 and CXCR4 in ARPE-19 cells at both mRNA and protein levels. Transfection with CXCR4 siRNAs decreased, while transfection with CXCR4 expression vector increased cell viability under high glucose treatment. We concluded that SDF-1/CXCR4 pathway improved diabetic retinopathy possibly by increasing cell viability.
It has been reported that lncRNA POU3F3 was upregulated in esophageal squamous-cell carcinomas, indicating its role as an oncogene in this disease. However, the mechanism of its function and its involvement in other malignancies is unknown. In the present study we found that expression levels of lncRNA POU3F3 were higher in tumor tissues than in adjacent healthy tissues of triple negative breast cancer (TNBC) patients and were significantly and inversely correlated with levels of cleaved caspase 9 only in tumor tissues. In addition, plasma levels of lncRNA POU3F3 were higher in TNBC patients than in healthy controls and were significantly and inversely correlated with levels of cleaved caspase 9 only in TNBC patients. In addition, treatment of exogenous Cleaved Caspase-9 significantly attenuated the effects of lncRNA POU3F3 overexpression on cancer cell proliferation and apoptosis. lncRNA POU3F3 may promote proliferation and inhibit apoptosis of cancer cells in triple-negative breast cancer. 相似文献