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| 1 | Ostracod Biostratigraphy of the Late Cretaceous Qingshankou Formation in the Songliao Basin显示文摘ostracod biostratigraphic 研究从使用从在 Songliao 盆在迟了的白垩纪 Qingshankou 形成钻的五口选择的井拿的核心构造的合成的地质的节在 425 件样品上被执行。19 个 ostracod 地区的一个总数在形成, 3 最新被建立被建立, 3 被修订。19 个 ostracod 地区详细被描述。这研究在 Songliao 盆在油矿为详细 stratigraphic 部门和 Qingshankou 形成和 Gaotaizi 油水库的关联提供一个基础。 | ZHANG Zhili LIU Zhenwen WANG Baichang ZHANG Ying YE Dequan | 2007 | Acta Geologica Sinica(English Edition)2007，81，5： | 5 |
| 2 | Small changes huge impact: the role of thioredoxin 1 in the regulation of apoptosis by S-nitrosylation显示文摘氮的氧化物(没有) 是 apoptosis 的 bioregulator,它有 antiapoptotic 和 proapoptotic 功能。然而,为它的相反的生物效果负责的分子的机制充分没被理解。在蛋白质 S-nitrosylation 的学习的最近的进展可以提供新奇卓见进由号码发信号的 apoptotic 的规定而另外的蛋白质的 S-nitrosylation 例如 caspases 和 Bcl-2 ,禁止 apoptosis ,一些蛋白质的 S-nitrosylation 例如 glyceraldehyde-3-phosphate 脱氢酶和船边交货,刺激 apoptosis ,暗示这translational以后修正的生物功能的复杂性。而且, nitrosylation 和 denitrosylation 能被 thioredoxin 调整 1 (Trx1 ) 系统。研究显示出那 Trx1 任何一个 transnitrosylates,取决于在 Trx1 的不同半胱氨酸残余的氧化还原作用地位或 denitrosylates 特定的蛋白质。S-nitrosylated Trx1 的 Cys73 为它的 transnitrosylating 活动负责而在为它的 denitrosylating 活动的 Trx1 的 Cys32 的免费 thiol。在这 minireview,我们在在 Trx1 和 NO 目标之间的相互作用的理解提供概述,并且在调整 apoptosis 讨论调停 Trx1 的 S-nitrosylation 的角色和特定的蛋白质的 denitrosylation。 | Huili Li Ajun Wan Guoqiang Xu Dequan Ye | 2013 | Acta Biochimica et Biophysica Sinica2013，45，3： | 4 |
| 3 | Varicella-zoster virus ORF7 interacts with ORF53 and plays a role in its trans-Golgi network localization显示文摘Varicella-zoster virus(VZV) is a neurotropic alphaherpesvirus that causes chickenpox and shingles. ORF7 is an important virulence determinant of VZV in both human skin and nerve tissues,however, its specific function and involved molecular mechanism in VZV pathogenesis remain largely elusive. Previous yeast two-hybrid studies on intraviral protein-protein interaction network in herpesviruses have revealed that VZV ORF7 may interact with ORF53, which is a virtually unstudied but essential viral protein. The aim of this study is to identify and characterize VZV ORF53, and to investigate its relationship with ORF7. For this purpose, we prepared monoclonal antibodies against ORF53 and, for the first time, characterized it as a ~40 k Da viral protein predominantly localizing to the trans-Golgi network of the infected host cell. Next, we further confirmed the interaction between ORF7 and ORF53 by co-immunoprecipitation and co-localization studies in both plasmid-transfected and VZV-infected cells. Moreover, interestingly, we found that ORF53 lost its trans-Golgi network localization and became dispersed in the cytoplasm of host cells infected with an ORF7-deleted recombinant VZV, and thus ORF7 seems to play a role in normal subcellular localization of ORF53. Collectively, these results suggested that ORF7 and ORF53 may function as a complex during infection, which may be implicated in VZV pathogenesis. | Wei Wang Wenkun Fu Dequan Pan Linli Cai Jianghui Ye Jian Liu Che Liu Yuqiong Que Ningshao Xia Hua Zhu Tong Cheng | 2017 | Virologica Sinica2017，32，5： | 1 |
| 4 | Ultra-sensitive Dirac-point-based biosensing on terahertz metasurfaces comprising patterned graphene and perovskites显示文摘Biosensors are a focus of research on terahertz metasurfaces. However, reports of ultra-sensitive biosensors based on Dirac points are rare. Here, a new terahertz metasurface is proposed that consists of patterned graphene and perovskites. This serves as an ultra-sensitive Dirac-point-based biosensor for qualitative detection of sericin.Theoretically, sericin may make graphene n-doped and drive the Fermi level to shift from the valence band to the Dirac point, causing a dramatic decrease in conductivity. Correspondingly, the dielectric environment on the metasurface undergoes significant change, which is suited for ultra-sensitive biosensing. In addition, metal halide perovskites, which are up-to-date optoelectronic materials, have a positive effect on the phase during terahertz wave transmission. Thus, this sensor was used to successfully detect sericin with a detection limit of 780 pg/m L, achieved by changing the amplitude and phase. The detection limit of this sensor is as much as one order of magnitude lower than that of sensors in published works. These results show that the Dirac-pointbased biosensor is a promising platform for a wide range of ultra-sensitive and qualitative detection in biosensing and biological sciences. | Xin Yan Tengteng Li Guohong Ma Ju Gao Tongling Wang Haiyun Yao Maosheng Yang Lanju Liang Jing Li Jie Li Dequan Wei Meng Wang Yunxia Ye Xiaoxian Song Haiting Zhang Chao Ma Yunpeng Ren Xudong Ren Jianquan Yao | 2022 | Photonics Research2022，10，2： | 0 |
| 5 | Functionally diverse ligands modulate different activation states of the formyl peptide receptor 2,a G protein-coupled receptor显示文摘OBJECTIVE To identify the mechanisms by which the formyl peptide receptor 2(FPR2)mediates both inflammatory and anti-inflammatory signaling in an agonist-dependent manner.METHODS Cells expressing FPR2 were incubated with weak agonists,Aβ42 and Ac2-26,before stimulation with a strong agonist,WKYMVm.Calcium mobilization,c AMP inhibition and MAP kinase activation were measured.Intramolecular FRET were determined using FPR2 constructs with an ECFP attached to the C-terminus and a Fl As H binding motif embedded in the first or third intracellular loop(IL1 or IL3,respectively).RESULTS Aβ42 did not induce significant Ca^(2+) mobilization,but positively modulated WKYMVm-induced Ca^(2+) mobilization and c AMP reduction in a dose-variable manner within a narrow range of ligand concentrations.Treating FPR2-expressing cells with Ac2-26,a peptide with anti-inflammatory activity,negatively modulated WKYMVm-induced Ca^(2+) mobilization and c AMP reduction.Intramolecular FRET assay showed that stimulation of the receptor constructs with Aβ42 brought the C-terminal domain closer to IL1 but away from IL3.An opposite conformational change was induced by Ac2-26.The FPR2 conformation induced by Aβ42 corresponded to enhanced ERK phosphorylation and attenuated p38 MAPK phosphorylation,whereas Ac2-26 induced FPR2 conformational change corresponding to elevated p38 MAPK phosphorylation and reduced ERK phosphorylation.CONCLUSION Aβ42 and Ac2-26 induce different conformational changes in FPR2.These findings provide a structural basis for FPR2 mediation of inflammatory vs anti-inflammatory functions and identify a type of receptor modulation that differs from the classic positive and negative allosteric modulation. | Shuo ZHANG Hao GONG Richard Dequan YE | 2017 | 中国药理学与毒理学杂志2017，31，10： | 0 |
| 6 | Biphasic modulation of chemerin peptide-induced calcium flux and ERK phosphorylation by amyloid beta peptide显示文摘OBJECTIVE The chemokine-like receptor 1(CMKLR1,Chem R23) is a functional receptor for chemerin,the chemerin-derived nonapeptide(C9),and the amyloid β peptide 1-42(Aβ_(42)).Because these peptides share little sequence homology,studies were conducted to investigate their pharmacological properties and regulation at CMKLR1.METHODS Cells expressing CMKLR1 were incubated with Aβ_(42) before stimulation with a strong agonist,the C9 peptide.Calcium mobilization,c AMP inhibition and MAP kinase activation were measured.Intramolecular FRET were determined using CMKLR1 constructs with an ECFP attached to the C-terminus and a Fl As H binding motif embedded in the first intracellular loop(IL1).RESULTS Binding of both Aβ_(42) and the C9 peptide induced CMKLR1 internalization,but only the Aβ_(42)-induced receptor internalization involved clathrin-coated pits.Likewise,Aβ_(42) but not C9 stimulated β-arrestin 2 translocation to plasma membranes.A robust Ca^(2+)flux was observed following C9 stimulation,whereas Aβ_(42) was ineffective even at micromolar concentrations.Despite its low potency in calcium mobilization assay,Aβ_(42) was able to alter C9-induced Ca^(2+) flux in dose-dependent manner:a potentiation effect at 100 pmol·L^(-1) of Aβ_(42) was followed by a suppression at 10 nmol·L^(-1) and further potentiation at 1 μmol·L^(-1).This unusual and biphasic modulatory effect was also seen in the C9-induced ERK phosphorylation but the dose curve was opposite to that of Ca^(2+) flux and c AMP inhibition,suggesting a reciprocal regulatory mechanism.Intramolecular FRET assay confirmed that Aβ_(42) modulates CMKLR1 rather than its downstream signaling pathways.CONCLUSION These findings suggest Aβ_(42) as an allosteric modulator that can both positively and negatively regulate the activation state of CMKLR1 in a manner that differs from existing allosteric modulatory mechanisms. | Hao GONG Shuo ZHANG Dan LIAO Richard Dequan YE | 2017 | 中国药理学与毒理学杂志2017，31，10： | 0 |
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