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| 1 | The crystal structure of Ac-AChBP in complex with α-conotoxin LvlA reveals the mechanism of its selectivity towards different nAChR subtypes显示文摘3* nAChRs,被认为为象疼痛那样的问题正在答应药目标,嗜好,心血管的功能,认知混乱等等,在整个中央、外部的神经系统被发现。-conotoxin (-CTx) LvIA 作为迄今为止知道的 32 nAChRs 的最选择的禁止者被识别了,并且它能把 32 nAChR 子类型与 6/323 和 34 种 nAChR 子类型区分开来。然而,它向 32 的选择的机制, 6/323,和 34 nAChRs 留下逃犯。这里,我们在 3.4 的一个决定与 Aplysia californica 醋胆素绑定蛋白质(Ac-AChBP ) 在建筑群报导 LvIA 的合作水晶结构 ? 。基于这建筑群的结构,和基于另外的 nAChR 子类型和有约束力的亲密关系试金当模特儿的相同,我们断定 LvIA 的 Asp-11 在选择起一个重要作用向 32 的 LvIA 和由做盐的 3/623 nAChRs 与老鼠的 Lys-155 衔接 3 子单元。在被老鼠的 Met-36, Thr-59,和 Phe-119 形成的一个恐水病的衣袋以内的 Asn-9 谎言在 32 nAChR 模型的 2 子单元,向 32 nAChR 子类型为它的更多的有势力选择揭示原因。这些结果提供能被用来设计 ligands 的分子的卓见有选择地指向 32 nAChRs,与为新治疗学的 -CTxs 的设计的重要含意。 | Manyu Xu Xiaopeng Zhu Jinfang Yu Jinpeng Yu Sulan Luo Xinquan Wang | 2017 | Protein & Cell2017，8，9： | 3 |
| 2 | Thermodynamic activities of silicon and boron in Fe-Si-B ternary melts at 1 450 ℃显示文摘 | JI Chunlin YU Rongxiang LIU Sulan | 1988 | Canadian Metallurgical Quarterly1988，27，1： | 1 |
| 3 | Aryl hydrocarbon receptor activation drives polymorphonuclear myeloid-derived suppressor cell response and efficiently attenuates experimental Sjögren’s syndrome显示文摘Myeloid-derived suppressor cells(MDSCs)comprise heterogeneous myeloid cell populations with immunosuppressive capacity that contribute to immune regulation and tolerance induction.We previously reported impaired MDSC function in patients with primary Sjögren’s syndrome(pSS)and mice with experimental SS(ESS).However,the molecular mechanisms underlying MDSC dysfunction remain largely unclear.In this study,we first found that aryl hydrocarbon receptor(AhR)was highly expressed by human and murine polymorphonuclear MDSCs(PMN-MDSCs).Indole-3-propionic acid(IPA),a natural AhR ligand produced from dietary tryptophan,significantly promoted PMN-MDSC differentiation and suppressive function on CD4^(+)T cells.In contrast,feeding a tryptophan-free diet resulted in a decreased PMN-MDSC response,a phenotype that could be reversed by IPA supplementation.The functional importance of PMN-MDSCs was demonstrated in ESS mice by using a cell-depletion approach.Notably,AhR expression was reduced in PMN-MDSCs during ESS development,while AhR antagonism resulted in exacerbated ESS pathology and dysregulated T effector cells,which could be phenocopied by a tryptophan-free diet.Interferon regulatory factor 4(IRF4),a repressive transcription factor,was upregulated in PMN-MDSCs during ESS progression.Chromatin immunoprecipitation analysis revealed that IRF4 could bind to the promoter region of AhR,while IRF4 deficiency markedly enhanced AhR-mediated PMN-MDSC responses.Furthermore,dietary supplementation with IPA markedly ameliorated salivary glandular pathology in ESS mice with restored MDSC immunosuppressive function.Together,our results identify a novel function of AhR in modulating the PMN-MDSC response and demonstrate the therapeutic potential of targeting AhR for the treatment of pSS. | Yanxia Wei Na Peng Chong Deng Futao Zhao Jie Tian Yuan Tang Sulan Yu Yacun Chen Yu Xue Fan Xiao Yingbo Zhou Xiaomei Li Hejian Zou Ke Rui Xiang Lin Liwei Lu | 2022 | Cellular & Molecular Immunology2022，19，12： | 1 |
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