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71.
Xin Lu JianFeng Liu WeiXuan Fu JiaPeng Zhou YanRu Luo XiangDong Ding Yang Liu Qin Zhang 《PloS one》2013,8(10)
Increased disease resistance through improved immune capacity would be beneficial for the welfare and productivity of farm animals. To identify genomic regions responsible for immune capacity traits in swine, a genome-wide association study was conducted. In total, 675 pigs were included. At 21 days of age, all piglets were vaccinated with modified live classical swine fever vaccine. Blood samples were sampled when the piglets were 20 and 35 days of age, respectively. Four traits, including Interferon-gamma (IFN-γ) and Interleukin 10 (IL-10) levels, the ratio of IFN-γ to IL-10 and Immunoglobulin G (IgG) blocking percentage to CSFV in serum were measured. All the samples were genotyped for 62,163 single nucleotide polymorphisms (SNP) using the Illumina porcineSNP60k BeadChip. After quality control, 46,079 SNPs were selected for association tests based on a single-locus regression model. To tackle the issue of multiple testing, 10,000 permutations were performed to determine the chromosome-wise and genome-wise significance level. In total, 32 SNPs with chromosome-wise significance level (including 4 SNPs with genome-wise significance level) were identified. These SNPs account for 3.23% to 13.81% of the total phenotypic variance individually. For the four traits, the numbers of significant SNPs range from 5 to 15, which jointly account for 37.52%, 82.94%, 26.74% and 24.16% of the total phenotypic variance of IFN-γ, IL-10, IFN-γ/IL-10, and IgG, respectively. Several significant SNPs are located within the QTL regions reported in previous studies. Furthermore, several significant SNPs fall into the regions which harbour a number of known immunity-related genes. Results herein lay a preliminary foundation for further identifying the causal mutations affecting swine immune capacity in follow-up studies. 相似文献
72.
Colin F. Greineder Ann-Marie Chacko Sergei Zaytsev Blaine J. Zern Ronald Carnemolla Elizabeth D. Hood Jingyan Han Bi-Sen Ding Charles T. Esmon Vladimir R. Muzykantov 《PloS one》2013,8(11)
The use of targeted therapeutics to replenish pathologically deficient proteins on the luminal endothelial membrane has the potential to revolutionize emergency and cardiovascular medicine. Untargeted recombinant proteins, like activated protein C (APC) and thrombomodulin (TM), have demonstrated beneficial effects in acute vascular disorders, but have failed to have a major impact on clinical care. We recently reported that TM fused with an scFv antibody fragment to platelet endothelial cell adhesion molecule-1 (PECAM-1) exerts therapeutic effects superior to untargeted TM. PECAM-1 is localized to cell-cell junctions, however, whereas the endothelial protein C receptor (EPCR), the key co-factor of TM/APC, is exposed in the apical membrane. Here we tested whether anchoring TM to the intercellular adhesion molecule (ICAM-1) favors scFv/TM collaboration with EPCR. Indeed: i) endothelial targeting scFv/TM to ICAM-1 provides ∼15-fold greater activation of protein C than its PECAM-targeted counterpart; ii) blocking EPCR reduces protein C activation by scFv/TM anchored to endothelial ICAM-1, but not PECAM-1; and iii) anti-ICAM scFv/TM fusion provides more profound anti-inflammatory effects than anti-PECAM scFv/TM in a mouse model of acute lung injury. These findings, obtained using new translational constructs, emphasize the importance of targeting protein therapeutics to the proper surface determinant, in order to optimize their microenvironment and beneficial effects. 相似文献
73.
Zizhen Yao Cindy T.J. van Velthoven Thuc Nghi Nguyen Jeff Goldy Adriana E. Sedeno-Cortes Fahimeh Baftizadeh Darren Bertagnolli Tamara Casper Megan Chiang Kirsten Crichton Song-Lin Ding Olivia Fong Emma Garren Alexandra Glandon Nathan W. Gouwens James Gray Lucas T. Graybuck Michael J. Hawrylycz Hongkui Zeng 《Cell》2021,184(12):3222-3241.e26
74.
75.
Wenyi Yan a bc Shenghai Ye b Qingsheng Jin b Longjun Zeng c Yu Peng c Dawei Yan c Weibing Yang c Donglei Yang c Zuhua He c Yanjun Dong a Xiaoming Zhang b a College of Life Environment Sciences Shanghai Normal University Shanghai China b Institute of Crop Nuclear Technology Utilization Zhejiang Academy of Agricultural Sciences Hangzhou China c Institute of Plant Physiology & Ecology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai China 《Acta Genetica Sinica》2010,(1)
Plant senescence plays diverse important roles in development and environmental responses.However,the molecular basis of plant senescence is remained largely unknown.A rice spontaneous mutant with the character of early senescence and male sterility (sms) was found in the breeding line NT10-748.In order to identify the gene SMS1 and the underlying mechanism,we preliminarily analyzed physiological and biochemical phenotypes of the mutant.The mutant contained lower chlorophyll content compared with the wild t... 相似文献
76.
Iron–sulfur clusters are one of the most ubiquitous redox centers in biology. Ironically, iron-sulfur clusters are highly
sensitive to reactive oxygen species. Disruption of iron-sulfur clusters will not only change the activity of proteins that
host iron–sulfur clusters, the iron released from the disrupted iron–sulfur clusters will further promote the production of
deleterious hydroxyl free radicals via the Fenton reaction. Here, we report that ferritin A (FtnA), a major iron-storage protein
in Escherichia coli, is able to scavenge the iron released from the disrupted iron–sulfur clusters and alleviates the production of hydroxyl
free radicals. Furthermore, we find that the iron stored in FtnA can be retrieved by an iron chaperon IscA for the re-assembly
of the iron–sulfur cluster in a proposed scaffold IscU in the presence of the thioredoxin reductase system which emulates
normal intracellular redox potential. The results suggest that E. coli FtnA may act as an iron buffer to sequester the iron released from the disrupted iron–sulfur clusters under oxidative stress
conditions and to facilitate the re-assembly of the disrupted iron–sulfur clusters under normal physiological conditions. 相似文献
77.
Junfeng Dou Wei Qin Jing Yuan Aizhong Ding En Xie Yingying Wang 《Bioremediation Journal》2014,18(3):248-257
A pure strain of Microbacterium lacticum DJ-1 capable of anaer-obic biodegradation of ethylbenzene was isolated from soil contaminated with gasoline. Growth of the strain and biodegradation of ethylbenzene in batch cultures led to stoichiometric reduction of nitrate. M. lacticum DJ-1 could degrade 100 mg L?1 of ethylbenzene completely, with a maximum degradation rate of 15.02 ± 1.14 mg L?1 day?1. Increasing the initial concentration of ethy-lbenzene resulted in decreased degradative ability. The cell-specific growth rates on ethylbenzene conformed to the Haldane–Andrew model in the substrate level range of 10–150 mg L?1. Kinetic parameters were determined by nonlinear regression on specific growth rates and various initial substrate concentrat-ions, and the values of the maximum specific growth rate, half saturation constant, and inhibition constant were 0.71 day?1, 34.3 mg L?1, and 183.5 mg L?1, respectively. This is the first report of ethylbenzene biodegradation by a bacterium of Microbacterium lacticum under nitrate-reducing conditions. 相似文献
78.
79.
Fang Ma Meng-Ge Ding Yi-Yu Lei Li-Hua Luo Shun Jiang Yu-Hua Feng Xian-Ling Liu 《Cell death & disease》2020,11(12)
Immune escape is an important mechanism in tumorigenesis. The aim of this study was to investigate roles of SKIL in tumorigenesis and immune escape of non-small-cell lung cancer (NSCLC). SKIL expression levels in NSCLC cell line, clinical sample, and adjacent normal tissue were measured by quantitative PCR, western blot, or immunohistochemistry. Lentivirus was used to overexpress/silence SKIL or TAZ expression. Malignant phenotypes of NSCLC cells were evaluated by colony formation, transwell, and MTT assays, and in xenograft mice model. Syngeneic mice model and flow cytometry were used to evaluate T cell infiltration. Quantitative PCR and western blot were applied to evaluate relevant mRNA and protein levels, respectively. Co-immunoprecipitation was applied to unveil the interaction between SKIL and TAZ. SKIL expression was higher in NSCLC tissue compared to adjacent normal tissue. Silencing of SKIL inhibited malignant phenotypes of NSCLC cells and promoted T cell infiltration. SKIL-knockdown inhibited autophagy and activated the STING pathway in NSCLC cells through down-regulation of TAZ. Silencing of TAZ cancelled the effects of SKIL overexpression on malignant phenotypes and autophagy of NSCLC cells. Inhibition of autophagy reversed the effects of SKIL/TAZ overexpression on the STING pathway. In conclusion, SKIL promoted tumorigenesis and immune escape of NSCLC cells through upregulation of TAZ/autophagy axis and inhibition on downstream STING pathway.Subject terms: Immunology, Cancer 相似文献
80.