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| 1 | 2019新型冠状病毒基因组特征和流行病学:病毒起源和受体结合的意义显示文摘研究者对来自9例新型冠状病毒肺炎住院患者的支气管肺泡灌洗液样本和培养的分离株进行了下一代测序。从这些个体中获得了严重急性呼吸综合征-冠状病毒2(severe acute respiratory syndrome-coronavirus 2,SARS-CoV-2)的完整和部分基因组序列。利用Sanger测序连接病毒重叠群以获得全长基因组,cDNA末端快速扩增确定终端区。对这些SARSCoV-2基因组和其他冠状病毒基因组进行了系统进化分析,以确定该病毒的进化史并有助于推断其可能的起源。 | 刘青(译) 刘莉(审校) Lu R Zhao X Li J Niu P Yang B Wu H Wang W Song H Huang B Zhu N Bi Y Ma X Zhan F Wang L Hu T Zhou H Hu Z Zhou W Zhao L Chen J Meng Y Wang J Lin Y Yuan J Xie Z Ma J Liu WJ Wang D Xu W Holmes EC Gao GF Wu G Chen W Shi W Tan W | 2020 | 中华高血压杂志2020,28,3: | 516 |
| 2 | Androgen receptor: structure, role in prostate cancer and drug discovery显示文摘Androgens and androgen receptors (AR) play a pivotal role in expression of the male phenotype. Several diseases, such as androgen insensitivity syndrome (AIS) and prostate cancer, are associated with alterations in AR functions. Indeed, androgen blockade by drugs that prevent the production of androgens and/or block the action of the AR inhibits prostate cancer growth. However, resistance to these drugs often occurs after 2-3 years as the patients develop castration-resistant prostate cancer (CRPC). In CRPC, a functional AR remains a key regulator. Early studies focused on the functional domains of the AR and its crucial role in the pathology. The elucidation of the structures of the AR DNA binding domain (DBD) and ligand binding domain (LBD) provides a new framework for understanding the functions of this receptor and leads to the development of rational drug design for the treatment of prostate cancer. An overview of androgen receptor structure and activity, its actions in prostate cancer, and how structural information and high-throughput screening have been or can be used for drug discovery are provided herein. | MH Eileen TAN Jun LI H Eric XU Karsten MELCHER Eu-leong YONG | 2015 | Acta Pharmacologica Sinica2015,36,1: | 39 |
| 3 | Amyloid beta: structure, biology and structure-based therapeutic development显示文摘淀粉的贝它肽(A) 通过 transmembrane 蛋白质的解朊的处理被生产,淀粉的先锋蛋白质(应用软件) ,由 - 并且 -secretases。在大脑的累积被建议是在 Alzheimers 疾病的致病的一个早有毒的事件,它是在大脑与匾和混乱联系的痴呆的最普通的形式。当前, A 的生理、病理学的形式是什么,是不清楚的并且由由什么机制, A 引起痴呆。而且,没有有效的药停止或逆行 Alzheimers 的前进疾病。在这份报纸,我们考察 A 的结构,生物功能,和 neurotoxicity 角色。我们也讨论与 A 交往并且调停的潜在的受体吸入,清理,和新陈代谢。另外,我们为治疗 Alzheimers 疾病总结治疗学的开发和不同策略的最近的进展。最后,我们将在象为 Alzheimers 疾病的治疗答应策略选择一样寻找新奇、潜在地有效的代理人在进步上报导。这些前景包括对 A,它的受体和字形物蛋白质起作用的代理人,例如对 A 的小分子,疫苗和抗体;禁止者或调节的人 - 并且 -secretase;降级 A 的朊酶;字形物蛋白质禁止者和疫苗;淀粉的染料和 microRNAs。 | Guo-fang CHEN Ting-hai XU Yan YAN Yu-ren ZHOU Yi JIANG Karsten MELCHER H Eric XU | 2017 | Acta Pharmacologica Sinica2017,38,9: | 39 |
| 4 | Study of BESIII trigger efficiencies with the 2018 J/ψ data显示文摘Using a dedicated data sample taken in 2018 on the J/ψpeak,we perform a detailed study of the trigger efficiencies of the BESIII detector.The efficiencies are determined from three representative physics processes,namely Bhabha scattering,dimuon production and generic hadronic events with charged particles.The combined efficiency of all active triggers approaches 100%in most cases,with uncertainties small enough not to affect most physics analyses. | M.Ablikim M.N.Achasov P.Adlarson S.Ahmed M.Albrecht R.Aliberti A.Amoroso M.R.An Q.An X.H.Bai Y.Bai O.Bakina R.Baldini Ferroli I.Balossino Y.Ban K.Begzsuren N.Berger M.Bertani D.Bettoni F.Bianchi J.Bloms A.Bortone I.Boyko R.A.Briere H.Cai X.Cai A.Calcaterra G.F.Cao N.Cao S.A.Cetin J.F.Chang W.L.Chang G.Chelkov D.Y.Chen G.Chen H.S.Chen M.L.Chen S.J.Chen X.R.Chen Y.B.Chen Z.J Chen W.S.Cheng G.Cibinetto F.Cossio X.F.Cui H.L.Dai X.C.Dai A.Dbeyssi R.E.de Boer D.Dedovich Z.Y.Deng A.Denig I.Denysenko M.Destefanis F.De Mori Y.Ding C.Dong J.Dong L.Y.Dong M.Y.Dong X.Dong S.X.Du Y.L.Fan J.Fang S.S.Fang Y.Fang R.Farinelli L.Fava F.Feldbauer G.Felici C.Q.Feng J.H.Feng M.Fritsch C.D.Fu Y.Gao Y.Gao Y.Gao Y.G.Gao I.Garzia P.T.Ge C.Geng E.M.Gersabeck A Gilman K.Goetzen L.Gong W.X.Gong W.Gradl M.Greco L.M.Gu M.H.Gu S.Gu Y.T.Gu C.Y Guan A.Q.Guo L.B.Guo R.P.Guo Y.P.Guo A.Guskov T.T.Han W.Y.Han X.Q.Hao F.A.Harris H Hüsken K.L.He F.H.Heinsius C.H.Heinz T.Held Y.K.Heng C.Herold M.Himmelreich T.Holtmann Y.R.Hou Z.L.Hou H.M.Hu J.F.Hu T.Hu Y.Hu G.S.Huang L.Q.Huang X.T.Huang Y.P.Huang Z.Huang T.Hussain W.Ikegami Andersson W.Imoehl M.Irshad S.Jaeger S.Janchiv Q.Ji Q.P.Ji X.B.Ji X.L.Ji H.B.Jiang X.S.Jiang J.B.Jiao Z.Jiao S.Jin Y.Jin T.Johansson N.Kalantar-Nayestanaki X.S.Kang R.Kappert M.Kavatsyuk B.C.Ke I.K.Keshk A.Khoukaz P.Kiese R.Kiuchi R.Kliemt L.Koch O.B.Kolcu B.Kopf M.Kuemmel M.Kuessner A.Kupsc M.G.Kurth W.Kühn J.J.Lane J.S.Lange P.Larin A.Lavania L.Lavezzi Z.H.Lei H.Leithoff M.Lellmann T.Lenz C.Li C.H.Li Cheng Li D.M.Li F.Li G.Li H.Li H.Li H.B.Li H.J.Li J.L.Li J.Q.Li J.S.Li Ke Li L.K.Li Lei Li P.R.Li S.Y.Li W.D.Li W.G.Li X.H.Li X.L.Li Z.Y.Li H.Liang H.Liang H.Liang Y.F.Liang Y.T.Liang L.Z.Liao J.Libby C.X.Lin B.J.Liu C.X.Liu D.Liu F.H.Liu Fang Liu Feng Liu H.B.Liu H.M.Liu Huanhuan Liu Huihui Liu J.B.Liu J.L.Liu J.Y.Liu K.Liu K.Y.Liu Ke Liu L.Liu M.H.Liu P.L.Liu Q.Liu Q.Liu S.B.Liu Shuai Liu T.Liu W.M.Liu X.Liu Y.Liu Y.B.Liu Z.A.Liu Z.Q.Liu X.C.Lou F.X.Lu H.J.Lu J.D.Lu J.G.Lu X.L.Lu Y.Lu Y.P.Lu C.L.Luo M.X.Luo b P.W.Luo T.Luo X.L.Luo S.Lusso X.R.Lyu F.C.Ma H.L.Ma L.L.Ma M.M.Ma Q.M.Ma R.Q.Ma R.T.Ma X.X.Ma X.Y.Ma F.E.Maas M.Maggiora S.Maldaner S.Malde Q.A.Malik A.Mangoni Y.J.Mao Z.P.Mao S.Marcello Z.X.Meng J.G.Messchendorp G.Mezzadri T.J.Min R.E.Mitchell X.H.Mo Y.J.Mo N.Yu.Muchnoi H.Muramatsu S.Nakhoul Y.Nefedov F.Nerling I.B.Nikolaev Z.Ning S.Nisar S.L.Olsen Q.Ouyang S.Pacetti X.Pan Y.Pan A.Pathak P.Patteri M.Pelizaeus H.P.Peng K.Peters J.Pettersson J.L.Ping R.G.Ping R.Poling V.Prasad H.Qi H.R.Qi K.H.Qi M.Qi T.Y.Qi T.Y.Qi S.Qian W.-B.Qian Z.Qian C.F.Qiao L.Q.Qin X.S.Qin Z.H.Qin J.F.Qiu S.Q.Qu K.H.Rashid K.Ravindran C.F.Redmer A.Rivetti V.Rodin M.Rolo G.Rong Ch.Rosner M.Rump H.S.Sang A.Sarantsev Y.Schelhaas C.Schnier K.Schoenning M.Scodeggio D.C.Shan W.Shan X.Y.Shan J.F.Shangguan M.Shao C.P.Shen P.X.Shen X.Y.Shen H.C.Shi R.S.Shi X.Shi X.D Shi W.M.Song Y.X.Song S.Sosio S.Spataro K.X.Su P.P.Su F.F.Sui G.X.Sun H.K.Sun J.F.Sun L.Sun S.S.Sun T.Sun W.Y.Sun X Sun Y.J.Sun Y.K.Sun Y.Z.Sun Z.T.Sun Y.H.Tan Y.X.Tan C.J.Tang G.Y.Tang J.Tang J.X.Teng V.Thoren I.Uman B.Wang C.W.Wang D.Y.Wang H.J.Wang H.P.Wang K.Wang L.L.Wang M.Wang M.Z.Wang Meng Wang W.Wang W.H.Wang W.P.Wang X.Wang X.F.Wang X.L.Wang Y.Wang Y.D.Wang Y.F.Wang Y.Q.Wang Y.Y.Wang Z.Wang Z.Y.Wang Ziyi Wang Zongyuan Wang D.H.Wei P.Weidenkaff F.Weidner S.P.Wen D.J.White U.Wiedner G.Wilkinson M.Wolke L.Wollenberg J.F.Wu L.H.Wu L.J.Wu X.Wu Z.Wu L.Xia H.Xiao S.Y.Xiao Z.J.Xiao X.H.Xie Y.G.Xie Y.H.Xie T.Y.Xing G.F.Xu Q.J.Xu W.Xu X.P.Xu F.Yan L.Yan W.B.Yan W.C.Yan Xu Yan H.J.Yang H.X.Yang L.Yang S.L.Yang Y.X.Yang Yifan Yang Zhi Yang M.Ye M.H.Ye J.H.Yin Z.Y.You B.X.Yu C.X.Yu G.Yu J.S.Yu T.Yu C.Z.Yuan L.Yuan X.Q.Yuan Y.Yuan Z.Y.Yuan C.X.Yue A.Yuncu A.A.Zafar Y.Zeng B.X.Zhang Guangyi Zhang H.Zhang H.H.Zhang H.Y.Zhang J.J.Zhang J.L.Zhang J.Q.Zhang J.W.Zhang J.Y.Zhang J.Z.Zhang Jianyu Zhang Jiawei Zhang L.Q.Zhang Lei Zhang S.Zhang S.F.Zhang Shulei Zhang X.D.Zhang X.Y.Zhang Y.Zhang Y.H.Zhang Y.T.Zhang Yan Zhang Yao Zhang Yi Zhang Z.H.Zhang Z.Y.Zhang G.Zhao J.Zhao J.Y.Zhao J.Z.Zhao Lei Zhao Ling Zhao M.G.Zhao Q.Zhao S.J.Zhao Y.B.Zhao Y.X.Zhao Z.G.Zhao A.Zhemchugov B.Zheng J.P.Zheng Y.Zheng Y.H.Zheng B.Zhong C.Zhong L.P.Zhou Q.Zhou X.Zhou X.K.Zhou X.R.Zhou A.N.Zhu J.Zhu K.Zhu K.J.Zhu S.H.Zhu T.J.Zhu W.J.Zhu W.J.Zhu Y.C.Zhu Z.A.Zhu B.S.Zou J.H.Zou | 2021 | Chinese Physics C2021,45,2: | 33 |
| 5 | Examination of the therapeutic potential of Delta-24-RGD in brain tumor stem cells: role of autophagic cell death显示文摘 | Jiang H Gomez-Manzano C Aoki H Alonso MM Kondo S McCormick F Xu J Kondo Y Bekele BN Colman H Lang FF Fueyo J | 2007 | 中国神经肿瘤杂志2007,5,3: | 24 |
| 6 | Granulocyte-macrophage colony-stimulating factor (GM-CSF) and T-cell responses: what we do and don't know显示文摘Granulocyte 巨噬细胞刺激殖民地的因素(GM-CSF ) 是一个重要造血的生长因素和有免疫力的调节的人。GM-CSF 也在各种各样的传播白血球的功能的活动有深刻效果。它被许多房间类型在收到有免疫力的刺激之上包括 T 房间,巨噬细胞, endothelial 房间和成纤维细胞生产。尽管 GM-CSF 局部地被生产,它能以一种 paracrine 方式行动到在主人防卫提高他们的功能的成员传播 neutrophils,单核白血球和淋巴细胞。最近的集中的调查为它增加树枝状的房间(DC ) 成熟和功能以及巨噬细胞活动的能力作为一个有免疫力的助手在 GM-CSF 的应用程序上被集中。在经历化疗的癌症病人对待嗜中性白血球减少症临床上被使用,在在治疗期间的爱滋病病人,并且在在骨髓移植以后的病人。有趣地, GM-CSF-deficient 老鼠的造血的系统看起来正常;最重要的变化在一些特定的 T 房间回答。尽管 GM-CSF 的分子的克隆用 T 房间的 cDNA 图书馆被执行, T 房间在激活以后生产 GM-CSF,是众所周知的,在 T 房间功能上有在由 T 房间和它的效果的生产的这 cytokine 的系统的调查的缺乏。在这篇文章,我们将在 T 房间主要集中于 GM-CSF 的免疫生物学。 | Yufang Shi Catherine H Liu Arthur I Roberts Jyoti Das Guangwu Xu Guangwen Ren Yingyu Zhang Liying Zhang Zeng Rong Yuan Hung Sheng William Tan Gobardhan Das Satish Devadas | 2006 | Cell Research2006,16,2: | 22 |
| 7 | 体内腺相关病毒-常间回文重复序列丛集及其相关蛋白9介导的基因编辑可改善家族性高胆固醇血症的动脉粥样硬化显示文摘低密度脂蛋白受体(low-density lipoprotein receptor,Ldlr)基因突变是家族性高胆固醇血症的主要原因之一,可导致动脉粥样硬化,并具有很高的终生心血管病风险。常间回文重复序列丛集(clustered regularly interspaced short palindromic repeats,CRISPR)/CRISPR相关蛋白9(CRISPR-related protein 9,Cas9)系统是基因编辑纠正基因突变从而改善疾病的有效工具。该研究的目的是通过腺相关病毒(adeno-associated virus,AAV)携带的CRISPR/Cas9系统进行体内体细胞基因编辑,以确定其能否在小鼠模型中治疗由Ldlr突变体引起的家族性高胆固醇血症。 | 刘青(译) 叶鹏(审校) Zhao H Li Y He L Pu W Yu W Li Y Wu YT Xu C Wei Y Ding Q Song BL Huang H Zhou B | 2020 | 中华高血压杂志2020,28,3: | 22 |
| 8 | Unusual life-threatening Rosai-Dorfman disease of the trachea. role of NF-kappa B显示文摘 | Zhou, LF Chen, LA Zhu, QA Wang, C Xu, H Cui, XF Jiang, LF He, Ski Huang, M Yin, KS | 2010 | 南京医科大学学报(自然科学版)2010,30,11: | 21 |
| 9 | EZH2: biology, disease, and structure-based drug Jiscovery显示文摘 | Jin-zhi TAN Yan YAN Xiao-xi WANG Yi JIANG H Eric XU | 2014 | Acta Pharmacologica Sinica2014,35,2: | 21 |
| 10 | An ABA-mimicking ligand that reduces water loss and promotes drought resistance in plants显示文摘Abscisic 酸(骆驼毛的织物) 是最重要的荷尔蒙让植物抵抗干旱和另外的不能生活的压力。骆驼毛的织物直接绑在骆驼毛的织物受体的 PYR/PYL 家庭,导致类型 2C 磷酸酶(PP2C ) 和下游的骆驼毛的织物发信号的激活的抑制。骆驼毛的织物由小分子发信号的干预能帮助植物克服象干旱,寒冷和土壤咸度那样的不能生活的压力,这被想象。然而,由植物酶的化学不稳定性和快速的分解代谢限制骆驼毛的织物本身的实际申请。这里,我们报导一件小分子骆驼毛的织物的鉴定模仿(AM1 ) 那充当骆驼毛的织物受体的家庭的多重成员的有势力使活跃之物。在 Arabidopsis, AM1 激活高度类似于由骆驼毛的织物导致了那的一个基因网络。有 AM1 的处理禁止种子萌芽,阻止叶水损失,并且支持干旱抵抗。我们与 PYL2 骆驼毛的织物受体和 HAB1 PP2C 在建筑群解决了 AM1 的水晶结构,它表明 AM1 调停交往的 gate-latch-lock 网络,在骆驼毛的织物界限 receptor/PP2C 建筑群被保存的一个结构的特征。一起,这些结果证明一件单个小分子骆驼毛的织物模仿能激活多重骆驼毛的织物受体并且保护植物免受水损失和干旱应力的伤害。而且, AM1 复杂水晶结构为设计 ABA-mimicking 小分子的下一代提供一个结构的基础。 | Minjie Cao Xue Liu Yan Zhang Xiaoqian Xue X EdwardZhou Karsten Melcher Pan Gao Fuxing Wang Liang Zeng Yang Zhao Pan Deng Dafang Zhong Jian-Kang Zhu H Eric Xu Yong Xu | 2013 | Cell Research2013,23,8: | 17 |
| 11 | Association of farnesyl diphosphate synthase polymorphisms and response to alendronate treatment in Chinese postmenopausal women with osteoporosis显示文摘 | Liu Y Li M Zhou PR Xing XP Xia WB Xu L Liu H J Zhang ZL LiaoEY Chen DC Liu J Tao TZ Wu W | 2014 | Chinese Medical Journal2014,,4: | 16 |
| 12 | A delivery strategy for rotenone microspheres in an animal model of Parkinson's disease.显示文摘 | Huang J Liu H Gu W Yan Z Xu Z Yang Y Zhu X Li Y | 2006 | 中国生物学文摘2006,20,9: | 16 |
| 13 | Effects of endogenous beta-amyloid overproduction on tau phosphorylation in cell culture.显示文摘 | Wang ZF Li HL Li XC Zhang Q Tian Q Wang Q Xu H Wang JZ | 2006 | 中国生物学文摘2006,20,9: | 15 |
| 14 | 健康成人动脉粥样硬化斑块易感性和血栓形成的生物标志物变化与极端空气污染水平相关:北京AIRCHD研究显示文摘空气污染与心血管事件恶化的病理生理机制尚不完全清楚。该文探讨环境空气污染是否可以触发易损斑块.通过全身炎症途径促进血栓形成。方法:在北京AIRCHD研究中.2014-2016年间对73名健康成年人[年龄(23.3±5.4)岁]进行了随访。研究者使用线性混合效应模型评估了空气污染物与动脉粥样硬化斑块易损性、血栓形成和炎症相关生物标志物之间的关系,并使用中介效应分析(mediation analyses)探讨涉及的生物学途径。通过受试者工作特征(receiver operating characteristic,ROC)曲线分析评估每种生物标记物预测环境空气污染暴露的能力。 | 刘青 叶鹏 Xu H Wang T Liu S Brook RD Feng B Zhao Q Song X Yi T Chen J Zhang Y Wang Y Zheng L Rajagopalan S Li J Huang W | 2019 | 中华高血压杂志2019,27,4: | 13 |
| 15 | Bone tissue engineering via nanostructured calcium phosphate biomaterials and stem cells显示文摘Tissue engineering is promising to meet the increasing need for bone regeneration. Nanostructured calcium phosphate(CaP) biomaterials/scaffolds are of special interest as they share chemical/crystallographic similarities to inorganic components of bone. Three applications of nano-CaP are discussed in this review:nanostructured calcium phosphate cement(CPC); nano-CaP composites; and nano-CaP coatings. The interactions between stem cells and nano-CaP are highlighted, including cell attachment, orientation/morphology, differentiation and in vivo bone regeneration. Several trends can be seen:(i) nano-CaP biomaterials support stem cell attachment/proliferation and induce osteogenic differentiation, in some cases even without osteogenic supplements;(ii) the influence of nano-CaP surface patterns on cell alignment is not prominent due to non-uniform distribution of nano-crystals;(iii) nano-CaP can achieve better bone regeneration than conventional CaP biomaterials;(iv) combining stem cells with nano-CaP accelerates bone regeneration, the effect of which can be further enhanced by growth factors; and(v) cell microencapsulation in nano-CaP scaffolds is promising for bone tissue engineering. These understandings would help researchers to further uncover the underlying mechanisms and interactions in nano-CaP stem cell constructs in vitro and in vivo, tailor nano-CaP composite construct design and stem cell type selection to enhance cell function and bone regeneration, and translate laboratory findings to clinical treatments. | Ping Wang Liang Zhao Jason Liu Michael D Weir Xuedong Zhou Hockin H K Xu | 2014 | Bone Research2014,2,3: | 11 |
| 16 | Polymorphisms of MTHFD,plasma homocysteine levels, and risk of gastric cancer in ahigh-risk Chinese population显示文摘Purpose:Accumulative evidence suggests that folate has a protective effect on gastric cancer. The methylenetetrahyd-rofolate dlehydrogenase(MTHFD) plays an important role in folate and homocysteine metabolisms, and polymorphisms of MTHFD may result in disturbance of the folate-mediated homocysteine pathway. The aim of this study is to test the hypothesis that genetic variants of MTHFD and plasma homocysteine levels are associated with risk of gastric cancer and modulated by genotypes of methylenetetrahydrofolate reductase(MTHFR). Experimental Design: We genotyped G1958A and T401C in MTHFD and C677T in MTHFR and detected total plasma homocysteine(tHcy) levels in a case-control study of 589 gastric cancer cases and 635 cancer-free controls in a high-risk Chinese population. Results:The variant genotypes of MTHFD 1958AA and 401CC were associated with a significantly increased risk of gastric canceradjusted odds ratio(OR), 2.05; 95% confidence interval(95% CI),1.34-3.13 for 1958AA; adjusted OR,1.43; 95% CI,1.14-1.80 for 401CC compared with 1958GG/GA and 401TT/TC genotypes, respectively. Both of the effects were more evident in the subjects carrying MTHFR 677CT/TT genotypes. The average tHcy level was significantly higher in gastric cancer cases than in controls(P < 0.01), and the upper quartile of tHcy (> 13.6 mu mol/L) was associated with an 82% significantly increased risk of gastric cancer, compared with the lowest quartile of tHcy(<= 8.0 pmol/L;adjusted OR,1.82; 95% CI,1.20-2.75). Conclusions:The strong associations between MTHFD variants and the plasma tHcy levels and gastric cancer risk suggest, for the first time, a possible gene-environment interaction between genetic variants of folate-metabolizing genes and high tHcy levels in gastric carcinogenesis. | Wang, L. N Ke, Q Chen, W. S Wang, J. M Tan, Y. F Zhou, Y Hua, Z. L Ding, W. L Niu, J. Y Shen, J Zhang, Z. F Wang, X. R Xu, Y. H Shen, H. B Yi Xing | 2007 | 南京医科大学学报(自然科学版)2007,27,7: | 10 |
| 17 | Mechanosignaling activation of TGFβmaintains intervertebral disc homeostasis显示文摘Intervertebral disc(IVD) degeneration is the leading cause of disability with no disease-modifying treatment.IVD degeneration is associated with instable mechanical loading in the spine, but little is known about how mechanical stress regulates nucleus notochordal(NC) cells to maintain IVD homeostasis. Here we report that mechanical stress can result in excessive integrin α_vβ_6-mediated activation of transforming growth factor beta(TGFβ), decreased NC cell vacuoles, and increased matrix proteoglycan production, and results in degenerative disc disease(DDD). Knockout of TGFβ type II receptor(TβRII) or integrin α_v in the NC cells inhibited functional activity of postnatal NC cells and also resulted in DDD under mechanical loading.Administration of RGD peptide, TGFβ, and α_vβ_6-neutralizing antibodies attenuated IVD degeneration. Thus,integrin-mediated activation of TGFβ plays a critical role in mechanical signaling transduction to regulate IVD cell function and homeostasis. Manipulation of this signaling pathway may be a potential therapeutic target to modify DDD. | Qin Bian Lei Ma Amit Jain Janet L Crane Khaled Kebaish Mei Wan Zhengdong Zhang X Edward Guo Paul D Sponseller Cheryle A Seguin Lee H Riley Yongjun Wang Xu Cao | 2017 | Bone Research2017,5,1: | 9 |
| 18 | Structural basis of AMPK regulation by adenine nucleotides and glycogen显示文摘激活安培的蛋白质 kinase (AMPK ) 为糖尿病,肥胖,和癌症的治疗是一个中央细胞的精力传感器和精力动态平衡,和一个有希望的药目标的管理者。这里我们人的 α 的现在的低分辨率的水晶结构; 1 β 2 γ 1 holo-AMPK 建筑群跳了到它的 allosteric 调节的人安培和肝糖模仿 cyclodextrin,两个在 phosphorylated (4.05 Å) 并且 non-phosphorylated (4.60 Å) 状态。另外,我们解决了 2.95 Å人的 kinase 领域(KD ) 的结构跳了到邻近的 autoinhibitory 领域(帮助) 并且表现了广泛生物化学并且 mutational 研究。一起,这些研究由安培和肝糖说明 allosteric AMPK 调整的内在的机制,其绑定改变在交替的帮助(安培) 和糖类绑定模块(肝糖) 之间的 equilibria 相互作用。 | Xiaodan Li Lili Wang X Edward Zhou Jiyuan Ke Parker W de Waal Xin Gu M H Eileen Tan Dongye Wang Donghai Wu H Eric Xu Karsten Melcher | 2015 | Cell Research2015,25,1: | 8 |
| 19 | 内质网应激/微小RNA-26a负反馈调控回路调控非酒精性脂肪性肝病发生发展显示文摘[据Hepatology 2021年4月报道]题:内质网应激/微小RNA-26a负反馈调控回路调控非酒精性脂肪性肝病发生发展(作者Xu HX等)内质网应激是细胞应对内质网过载的适应性反应,广泛参与多种疾病的发生发展,包括以肝细胞脂质过度积累为典型特征的非酒精性脂肪性肝病(NAFLD),但内质网应激的内在调控机制目前尚不清楚。微小RNA(miRNA)在许多细胞应激反应中发挥重要功能,但其在内质网应激中的作用尚未系统研究。 | 徐海霞 傅湘辉 XU H TIAN Y TANG D | 2021 | 临床肝胆病杂志2021,37,7: | 7 |
| 20 | Destabilization of strigolactone receptor DWARF14 by binding of ligand and E3-1igase signaling effector DWARF3显示文摘 | Li-Hua Zhao X Edward Zhou Wei Yi Zhongshan Wu Yue Liu Yanyong Kang Li Hou Parker W de Waal Suling Li Yi Jiang Adrian Scaffidi Gavin R Flematti Steven M Smith Vinh Q Lam Patrick R Griffin YonghongWang Jiayang Li Karsten Melcher H Eric Xu | 2015 | Cell Research2015,25,11: | 7 |