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991.
Selective releasing intracellular product in Triton X-100 micelle aqueous solution to prepare whole cell biocatalyst is a novel strategy for biosynthesis of Monascus pigments, in which cell suspension culture exhibits some advantages comparing with the corresponding growing cell submerged culture. In the present work, the nonionic surfactant Triton X-100 was successfully replaced by edible plant oils for releasing intracellular Monascus pigments. High concentration of Monascus pigments (with absorbance nearly 710 AU at 470 nm in the oil phase, normalized to the aqueous phase volume approximately 142 AU) was achieved by cell suspension culture in peanut oil–water two-phase system. Furthermore, the utilization of edible oil as extractant also fulfills the demand for application of Monascus pigments as natural food colorant. 相似文献
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Alejandra Bernal Yanmei Hu Stephanie O. Palmer Aaron Silva James Bullard Yonghong Zhang 《Biomolecular NMR assignments》2016,10(2):249-252
Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen and a primary cause of infection in humans. P. aeruginosa can acquire resistance against multiple groups of antimicrobial agents, including β-lactams, aminoglycosides and fluoroquinolones, and multidrug resistance is increasing in this organism which makes treatment of the infections difficult and expensive. This has led to the unmet need for discovery of new compounds distinctly different from present antimicrobials. Protein synthesis is an essential metabolic process and a validated target for the development of new antibiotics. Translation initiation factor 1 from P. aeruginosa (Pa-IF1) is the smallest of the three initiation factors that acts to establish the 30S initiation complex to initiate translation during protein biosynthesis, and its structure is unknown. Here we report the 1H, 13C and 15N chemical shift assignments of Pa-IF1 as the basis for NMR structure determination and interaction studies. Secondary structure analyses deduced from the NMR chemical shift data have identified five β-strands with an unusually extended β-strand at the C-terminal end of the protein and one short α-helix arranged in the sequential order β1–β2–β3–α1–β4–β5. This is further supported by 15N–{1H} hetero NOEs. These secondary structure elements suggest the Pa-IF1 adopts the typical β-barrel structure and is composed of an oligomer-binding motif. 相似文献
995.
Facilitated long chain fatty acid uptake by adipocytes remains upregulated relative to BMI for more than a year after major bariatric surgical weight loss
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Fengxia Ge José L. Walewski Mehyar Hefazi Torghabeh Harrison Lobdell IV Chunguang Hu Shengli Zhou Gregory Dakin Alfons Pomp Marc Bessler Beth Schrope Aku Ude‐Welcome William B. Inabnet Tianshu Feng Elektra Carras‐Terzian Dieunine Anglade Faith E. Ebel Paul D. Berk 《Obesity (Silver Spring, Md.)》2016,24(1):113-122
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Jiandong Zheng Xixiang Huo Yang Huai Lin Xiao Hui Jiang John Klena Carolyn M. Greene Xuesen Xing Jigui Huang Shali Liu Youxing Peng Hui Yang Jun Luo Zhibin Peng Linlin Liu Maoyi Chen Hui Chen Yuzhi Zhang Danqin Huang Xuhua Guan Luzhao Feng Faxian Zhan Dale J. Hu Jay K. Varma Hongjie Yu 《PloS one》2016,11(3)
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Fengjuan Zhang Donghai Peng Chunsheng Cheng Wei Zhou Shouyong Ju Danfeng Wan Ziquan Yu Jianwei Shi Yaoyao Deng Fenshan Wang Xiaobo Ye Zhenfei Hu Jian Lin Lifang Ruan Ming Sun 《PLoS pathogens》2016,12(1)
Cell death plays an important role in host-pathogen interactions. Crystal proteins (toxins) are essential components of Bacillus thuringiensis (Bt) biological pesticides because of their specific toxicity against insects and nematodes. However, the mode of action by which crystal toxins to induce cell death is not completely understood. Here we show that crystal toxin triggers cell death by necrosis signaling pathway using crystal toxin Cry6Aa-Caenorhabditis elegans toxin-host interaction system, which involves an increase in concentrations of cytoplasmic calcium, lysosomal lyses, uptake of propidium iodide, and burst of death fluorescence. We find that a deficiency in the necrosis pathway confers tolerance to Cry6Aa toxin. Intriguingly, the necrosis pathway is specifically triggered by Cry6Aa, not by Cry5Ba, whose amino acid sequence is different from that of Cry6Aa. Furthermore, Cry6Aa-induced necrosis pathway requires aspartic protease (ASP-1). In addition, ASP-1 protects Cry6Aa from over-degradation in C. elegans. This is the first demonstration that deficiency in necrosis pathway confers tolerance to Bt crystal protein, and that Cry6A triggers necrosis represents a newly added necrosis paradigm in the C. elegans. Understanding this model could lead to new strategies for nematode control. 相似文献
999.
Yi-Juan Hu Peizhou Liao H. Richard Johnston Andrew S. Allen Glen A. Satten 《PLoS genetics》2016,12(5)
Next-generation sequencing of DNA provides an unprecedented opportunity to discover rare genetic variants associated with complex diseases and traits. However, the common practice of first calling underlying genotypes and then treating the called values as known is prone to false positive findings, especially when genotyping errors are systematically different between cases and controls. This happens whenever cases and controls are sequenced at different depths, on different platforms, or in different batches. In this article, we provide a likelihood-based approach to testing rare variant associations that directly models sequencing reads without calling genotypes. We consider the (weighted) burden test statistic, which is the (weighted) sum of the score statistic for assessing effects of individual variants on the trait of interest. Because variant locations are unknown, we develop a simple, computationally efficient screening algorithm to estimate the loci that are variants. Because our burden statistic may not have mean zero after screening, we develop a novel bootstrap procedure for assessing the significance of the burden statistic. We demonstrate through extensive simulation studies that the proposed tests are robust to a wide range of differential sequencing qualities between cases and controls, and are at least as powerful as the standard genotype calling approach when the latter controls type I error. An application to the UK10K data reveals novel rare variants in gene BTBD18 associated with childhood onset obesity. The relevant software is freely available. 相似文献
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