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7篇 您的检索式:作者名="Yuichiro D"
    题名 作者 年代 出处 被引量
1Reactivity of triglycerides and fatty acids of rapeseed oil in supercritical alcohols显示文摘 Kusdiana D Saka S 2004Bioresource Technology2004,91,:1
2Prognostic significance of heat shock proteins 27 and 70 in patients with squamous cell carcinoma of the esophagus显示文摘Kensyu K Hitoshi S Yuichiro D 1999Cancer1999,85,8:1
3Correlation between tumor blood flow assessed by perfusion CT and effect of neoadjuvant therapy in advanced esophageal cancers 显示文摘Yoichi M Takushi Y Yuichiro D 2007J Surg Oncol2007,96,3:1
4Head Module control of mediator interactions显示文摘Yuichiro Takagi Guillermo Calero Roger D Kornberg 2006Mol Cell2006,23,:1
5Prognostic significance of heat shock proteins 27 and 70 in patients with squamous cell carcinoma of the esophagus 显示文摘Kensyu K Hitoshi S Yuichiro D 1999Cancer1999,85,8:1
6Crystal structures of the TRIC trimeric intracellular cation channel orthologues显示文摘从 sarcoplasmic 蜂窝胃(SR ) 和 endoplasmic 蜂窝胃的 Ca 2+ 版本(嗯) 为肌肉收缩是关键的,细胞生长, apoptosis,学习并且记忆。trimeric 细胞内部的阳离子(TRIC ) 隧道最近作为平衡 SR 的阳离子隧道被识别并且嗯膜潜力,并且在 Ca 2+ 发信号和动态平衡被含有。这里我们在场处于关上的状态和原核生物、真核细胞的 TRIC 隧道的基于结构的功能的分析的原核生物的 TRIC 隧道的水晶结构。各更整齐的子单元由七 transmembrane (TM ) 组成有二的 helices 转换了重复区域。electrophysiological,揭示的生物化学、生物物理的分析 TRIC 隧道在每个子单元以内拥有一个进行离子的毛孔,并且更整齐的形成贡献蛋白质的稳定性。相称性地相关的 TM2 和 TM5 helices 是在保存 glycine 簇的 kinked,并且这些性变态为隧道活动是重要的。而且, TM2 和 TM5 helices 的性变态在每个子单元接口产生侧面的开窗术。出人意料地,这些侧面的开窗术与类脂化合物分子被占据。这研究为这个离子隧道总科的分子的机制提供结构、功能的框架。Go Kasuya Masahiro Hiraizumi Andres D Maturana Kaoru Kumazaki Yuichiro Fujiwara Keihong Liu Yoshiko Nakada-Nakura So Iwata Keisuke Tsukada Tomotaka Komori Sotaro Uemura Yuhei Goto Takanori Nakane Mizuki Takemoto Hideaki E Kato Keitaro Yamashita Miki Wada Koichi Ito Ryuichiro Ishitani Motoyuki Hattori Osamu Nureki 2016Cell Research2016,26,12:0
7Human IgG1 antibodies suppress angiogenesis in a target-independent manner显示文摘Aberrant angiogenesis is implicated in diseases affecting nearly 10%of the world’s population.The most widely used antiangiogenic drug is bevacizumab,a humanized IgG1 monoclonal antibody that targets human VEGFA.Although bevacizumab does not recognize mouse Vegfa,it inhibits angiogenesis in mice.Here we show bevacizumab suppressed angiogenesis in three mouse models not via Vegfa blockade but rather Fc-mediated signaling through FcγRI(CD64)and c-Cbl,impairing macrophage migration.Other approved humanized or human IgG1 antibodies without mouse targets(adalimumab,alemtuzumab,ofatumumab,omalizumab,palivizumab and tocilizumab),mouse IgG2a,and overexpression of human IgG1-Fc or mouse IgG2a-Fc,also inhibited angiogenesis in wild-type and FcγR humanized mice.This anti-angiogenic effect was abolished by Fcgr1 ablation or knockdown,Fc cleavage,IgG-Fc inhibition,disruption of Fc-FcγR interaction,or elimination of FcRγ-initated signaling.Furthermore,bevacizumab’s Fc region potentiated its anti-angiogenic activity in humanized VEGFA mice.Finally,mice deficient in FcγRI exhibited increased developmental and pathological angiogenesis.These findings reveal an unexpected anti-angiogenic function for FcγRI and a potentially concerning off-target effect of hIgG1 therapies.Sasha Bogdanovich Younghee Kim Takeshi Mizutani Reo Yasuma Laura Tudisco Valeria Cicatiello Ana Bastos-Carvalho Nagaraj Kerur Yoshio Hirano Judit Z Baffi Valeria Tarallo Shengjian Li Tetsuhiro Yasuma Parthasarathy Arpitha Benjamin J Fowler Charles B Wright Ivana Apicella Adelaide Greco Arturo Brunetti Menotti Ruvo Annamaria Sandomenico Miho Nozaki Ryo Ijima Hiroki Kaneko Yuichiro Ogura Hiroko Terasaki Balamurali K Ambati Jeanette HW Leusen Wallace Y Langdon Michael R Clark Kathryn L Armour Pierre Bruhns J Sjef Verbeek Bradley D Gelfand Sandro De Falco Jayakrishna Ambati 2016Signal Transduction and Targeted Therapy2016,1,1:0
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