603 research outputs found

    Casper Is a FADD- and Caspase-Related Inducer of Apoptosis

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    AbstractCaspases are cysteine proteases that play a central role in apoptosis. Caspase-8 may be the first enzyme of the proteolytic cascade activated by the Fas ligand and tumor necrosis factor (TNF). Caspase-8 is recruited to Fas and TNF receptor-1 (TNF-R1) through interaction of its prodomain with the death effector domain (DED) of the receptor-associating FADD. Here we describe a novel 55 kDa protein, Casper, that has sequence similarity to caspase-8 throughout its length. However, Casper is not a caspase since it lacks several conserved amino acids found in all caspases. Casper interacts with FADD, caspase-8, caspase-3, TRAF1, and TRAF2 through distinct domains. When overexpressed in mammalian cells, Casper potently induces apoptosis. A C-terminal deletion mutant of Casper inhibits TNF- and Fas-induced cell death, suggesting that Casper is involved in these apoptotic pathways

    Historical Review about Research on “Bonghan System” in China

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    The meridian-collateral theory is the theoretical basis of acupuncture-moxibustion therapy. Professor Bonghan Kim, a professor of the Pyongyang Medical University of the Democratic People’s Republic of Korea, claimed that he found the anatomical structure of meridian-collaterals, named Bonghan corpuscles (BHCs) and Bonghan ducts (BHDs) system or primo vascular system (PVS), in 1962. From 1963 to 1965, researchers from our institute conducted a series of comparative anatomical experiments, trying to reproduce the so-called BHC- and BHD-like structures in different strains of animals. In the present paper, the authors introduced their research findings about BHC- and BHD-like structures in the young rabbit’s umbilicus including its external appearance, ectoplasm and endoplasm, and about strip-like and node-like objects in the blood vessels and lymph vessels near the larger abdominal and cervical blood vessels and chromaffin tissue in the back wall of the rabbit’s abdominal cavity and between the bilateral kidneys. In spite of existence of the BHC- and BHD-like structures in the rabbit, there has been no proved evidence for their association with the meridian-collateral system described in acupuncture medicine. In the present historical review, the authors also make a discussion about the significance of those findings

    Glycogen Synthase Kinase 3β Regulates IRF3 Transcription Factor-Mediated Antiviral Response via Activation of the Kinase TBK1

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    SummaryViral infection activates transcription factors IRF3 and NF-κB, which collaborate to induce type I interferons (IFNs). Here, we identified glycogen synthase kinase 3β (GSK3β) as an important regulator for virus-triggered IRF3 and NF-κB activation, IFN-β induction, and cellular antiviral response. Overexpression of GSK3β potentiated virus-induced activation of IRF3 and transcription of the IFNB1 gene, whereas reduced expression or deletion of GSK3β impaired virus-induced IRF3 and NF-κB activation, transcription of the IFNB1 gene, as well as cellular antiviral response. GSK3β physically associated with the kinase TBK1 in a viral infection-dependent manner. GSK3β promoted TBK1 self-association and autophosphorylation at Ser172, which is critical for virus-induced IRF3 activation and IFN-β induction. The effect of GSK3β on virus-induced signaling is independent of its kinase activity. Our findings suggest that GSK3β plays important roles in virus-triggered IRF3 activation by promoting TBK1 activation and provide new insights to the molecular mechanisms of cellular antiviral response

    Poly[tetra­kis(2,2′-bipyridine)undeca-μ-oxido-hexa­oxidodicopper(II)hexa­vanadium(V)]

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    In the title organic–inorganic hybrid vanadate complex, [Cu2V6O17(C10H8N2)4]n, the CuII atom is six-coordinated by two chelating 2,2′-bipyridine (bipy) ligands and two vanadate O atoms in a distorted octa­hedral geometry. Two [Cu(bipy)2V3O8] units are linked by a bridging O atom, which lies on an inversion center, forming a dimeric unit. The dimeric units are further connected by bridging vanadate O atoms into a two-dimensional layer parallel to (100). The layers are connected by weak C—H⋯O hydrogen bonds

    The effects of afforestation on soil bacterial communities in temperate grassland are modulated by soil chemical properties

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    Grassland afforestation dramatically affects the abiotic, biotic, and ecological function properties of the original ecosystems. Interference from afforestation might disrupt the stasis of soil physicochemical properties and the dynamic balance of microbiota. Some studies have suggested low sensitivity of soil properties and bacterial community to afforestation, but the apparent lack of a significant relationship is probably due to the confounding effects of the generalist habitat and rare bacterial communities. In this study, soil chemical and prokaryotic properties in a 30-year-old Mongolia pine (Pinus sylvestris var. mongolica Litv.) afforested region and adjacent grassland in Inner Mongolia were classified and quantified. Our results indicate that the high richness of rare microbes accounts for the alpha-diversity of the soil microbiome. Few OTUs of generalist (core bacteria) and habitat-specialist bacteria are present. However, the high abundance of this small number of OTUs governs the beta-diversity of the grassland and afforested land bacterial communities. Afforestation has changed the soil chemical properties, thus indirectly affecting the soil bacterial composition rather than richness. The contents of soil P, Ca2+, and Fe3+ account for differentially abundant OTUs such as Planctomycetes and subsequent changes in the ecologically functional potential of soil bacterial communities due to grassland afforestation. We conclude that grassland afforestation has changed the chemical properties and composition of the soil and ecological functions of the soil bacterial community and that these effects of afforestation on the microbiome have been modulated by changes in soil chemical properties

    Exploration and practice of animal physiology teaching mode for top class

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    动物生理学是动物医学、动物科学专业的重要基础理论课程。针对本校拔尖班学生培养计划和学习特点,本课程在教学中注重情境化教学,把最新研究进展及时整合到相应教学模块中,适当提高过程性评价比例,探索出适合拔尖班学生的授课模式,改善教学效果。Animal physiology is an important basic theoretical course for the specialty of animal medicine and animal science. According to the training programs and learning characteristics of top class students in our college, this course focused on situational teaching, integrated the latest progress manner into teaching model timely, and properly increased the process evaluation proportion in order to explore suitable teaching mode for top-class students, and improve teaching effectiveness

    3′,6′-Bis(diethyl­amino)-2-phenyl­spiro[isoindoline-1,9′-xanthen]-3-one

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    The title compound, C34H35O2N3, was synthesized by the reaction of 2-[3,6-bis­(diethyl­amino)-9H-xanthen-9-yl]benzoyl chloride with aniline. In the mol­ecular structure, the dihedral angles between the isoindoline and xanthene planes and between the isoindoline and benzene planes are 86.9 (3) and 47.0 (2)°, respectively. The mol­ecular packing in the crystal structure is stabilized by weak C—H⋯O hydrogen bonding

    Reduced Competitiveness of Autoantigen-Engaged B Cells due to Increased Dependence on BAFF

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    AbstractPeripheral autoantigen binding B cells are poorly competitive with naive B cells for survival and undergo rapid cell death. However, in monoclonal Ig-transgenic mice lacking competitor B cells, autoantigen binding B cells can survive for extended periods. The basis for competitive elimination of autoantigen binding B cells has been unknown. Here we demonstrate that autoantigen binding B cells have increased dependence on BAFF for survival. In monoclonal Ig-transgenic mice, each autoantigen binding B cell receives elevated amounts of BAFF, exhibiting increased levels of NFκB p52 and of the prosurvival kinase Pim2. When placed in a diverse B cell compartment, BAFF receptor engagement and signaling are reduced and the autoantigen binding cells are unable to protect themselves from Bim and possibly other death-promoting factors induced by chronic BCR signaling. These findings indicate that under conditions where BAFF levels are elevated, autoantigen-engaged cells will be rescued from rapid competitive elimination, predisposing to the development of autoimmune disease
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