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| 1 | DOG 1.0: illustrator of protein domain structures显示文摘 | Jian Ren Longping Wen Xinjiao Gao Changjiang Jin Yu Xue Xuebiao Yao | 2009 | Cell Research2009，19，2： | 20 |
| 2 | Differential secretome analysis reveals CST6 as a suppressor of breast cancer bone metastasis显示文摘骨头转移从疾病是乳癌的经常的复杂并发症和病态和死亡的一个普通原因。在转移期间,分泌蛋白质在在癌症房间和主人基质之间的相互作用起关键作用。为了描绘分泌蛋白质,那与乳癌骨头转移被联系,我们比较四个 MDA-MB-231 (MDA231 ) 衍生物房间的 secretomes 的没有标签的 proteomic 分析与骨头转移的改变的能力衬里的 preformed。128 蛋白质的一个总数被发现是一致地在骨头回归线癌症房间的调节媒介的 up-/down-regulated。改变的蛋白质的充实的分子的函数包括了受体绑定和 peptidase 抑制。通过乳癌房间的另外的 transcriptomic 分析,我们选择了 cystatin E/M (CST6 ) ,在骨头变形的房间下面调整的一个半胱氨酸朊酶禁止者,为进一步功能的研究。我们的结果证明 CST6 压制了乳癌房间的增长,殖民地形成,迁居和侵略。对癌症房间活动性的镇压功能被癌症执行导出房间的可溶的 CST6。更重要地,在癌症房间的 CST6 的宫外的表示在动物学习救了老鼠免于公开 osteolytic 转移和死亡,当时 CST6 击倒的显著地提高的癌症房间骨头转移和弄短的动物幸存。总的来说,我们的学习提供了乳癌骨头向性的全身的 secretome 分析并且作为乳癌 osteolytic 转移的真正的 suppressor 建立了分泌 CST6。 | Lei Jin Yan Zhang Hui Li Ling Yao Da Fu Xuebiao Yao Lisa X Xu Xiaofang Hu Guohong Hu | 2012 | Cell Research2012，22，9： | 15 |
| 3 | Experimental cancer gene therapy by multiple anti-survivin hammerhead ribozymes显示文摘为癌症改进基因治疗的功效,我们设计了指向 survivin mRNA 的暴露的区域的四撞木鲛 ribozyme 侵入人体气管粘膜的病菌(到 R4 的 R1 ) 。除了在里面 vitro 描述,由教材扩展包括了劈开的顺序特性的一颗决心,为细胞增长并且为的试金在 vivo 肿瘤,生长被用来为 ribozyme 效率得分。survivin 表示的产生抑制经由 caspase-3-dependent 小径导致了有丝分裂的大祸和房间死亡。重要地, ribozyme 侵入人体气管粘膜的病菌的管理在一个 hepato 细胞的癌异种皮移植老鼠模型禁止了肿瘤生长。R1, R3 和 R4 ribozymes 的合作表示 synergistically 压制了 survivin 并且当这联合指向 survivin 抄本的所有主要形式,生产了大多数有势力反癌症效果。带在这份报告描述的多重撞木鲛 ribozymes 的侵入人体气管粘膜的病菌对癌症提供了柔韧的基因治疗策略。 | Qi Fei Hongyu Zhang Lili Fu Xinlan Dai Baomei Gao Min Ni Chao Ge Jinjun Li Xia Ding Yuwen Ke Xuebiao Yao Jingde Zhu | 2008 | Acta Biochimica et Biophysica Sinica2008，40，6： | 10 |
| 4 | Aurora A orchestrates entosis by regulating a dynamic MCAK-TIP150 interaction显示文摘 | PengXia JinhuaZhou Xiaoyu Song BingWu XingLiu Di Li Shuyuan Zhang Zhikai Wang H uijuan Yu Tarsha Ward Jiancun Zhang Yinmei Li Xiaoning Wang YongChen Zhen Guo Xuebiao Yao | 2014 | Journal of Molecular Cell Biology2014，8，3： | 9 |
| 5 | BubR1 phosphorylates CENP-E as a switch enabling the transition from lateral association to end-on capture of spindle microtubules显示文摘Error-free mitosis depends on accurate chromosome attachment to spindle microtubules, powered congression of those chromosomes, their segregation in anaphase, and assembly of a spindle midzone at mitotic exit. The centromere-associated kinesin motor CENP-E, whose binding partner is BubR1, has been implicated in congression of misaligned chromosomes and the transition from lateral kinetochore-microtubule association to end-on capture. Although previously proposed to be a pseudokinase, here we report the structure of the kinase domain of Drosophila melanogaster BubR1, revealing its folding into a conformation predicted to be catalytically active. BubR1 is shown to be a bona fide kinase whose phosphorylation of CENP-E switches it from a laterally attached microtubule motor to a plus-end microtubule tip tracker. Computational modeling is used to identify bubristatin as a selective BubR1 kinase antagonist that targets the αN1 helix of N-terminal extension and αC helix of the BubR1 kinase domain. Inhibition of CENP-E phosphorylation is shown to prevent proper microtubule capture at kinetochores and, surprisingly, proper assembly of the central spindle at mitotic exit. Thus, BubR1-mediated CENP-E phosphorylation produces a temporal switch that enables transition from lateral to end-on microtubule capture and organization of microtubules into stable midzone arrays. | Yuejia Huang Lin Lin Xing Liu Sheng Ye Phil Y. Yao Wenwen Wang Fengrui Yang Xinjiao Gao Junying Li Yin Zhang Jiancun Zhang Zhihong Yang Xu Liu Zhenye Yang Jianye Zang Maikun Teng Zhiyong Wang Ke Ruan Xia Ding Lin Li Don W. Cleveland Rongguang Zhang Xuebiao Yao | 2019 | Cell Research2019，29，7： | 8 |
| 6 | Probing CENP-E function in chromosome dynamics using small molecule inhibitor syntelin显示文摘 | Xia Ding Feng Yan Phil Yao Zhihong Yang Weihong Wan Xiwei Wang Jing Liu Xinjiao Gao Ariane Abrieu Tongge Zhu Jiancun Zhang Zhen Dou Xuebiao Yao | 2010 | Cell Research2010，20，12： | 8 |
| 7 | Mitosis-specific acetylation tunes Ran effector binding for chromosome segregation显示文摘在房间期间,分割要求忠诚有丝分裂的锭子汇编和染色体分离的基因信息的稳定的传播。运用了 GTPase 戏在有丝分裂的锭子汇编的一个关键角色。然而,在锭子的 Ran-GTP 的一个化学坡度的产生怎么被联合到有丝分裂的 translational 以后修正,从来没被描绘过。这里,我们解决了复杂结构与核苷酸版本因素 Mog1 跑了并且描出一个新奇有丝分裂特定的调整 acetylation 的 Ran-Mog1 相互作用在染色体分离期间。我们的指导结构的功能的分析表明那 Mog1 与 RCC1 竞争为以一种 GTP/GDP-dependent 方式变有约束力。生物化学的描述表明了那 Mog1 固定跑阻止 RCC1 有约束力、随后的 GTP 装载。令人惊讶地,跑了是 TIP60 的真正的底层,并且由 TIP60 的 Lys134 的 acetylation 解放 Mog1 从在有丝分裂期间变有约束力。重要地,这个得到 acetylation 的开关对 RCC1 变有约束力支持 Ran-GTP 的高水平,它为染色体排列是必要的。这些结果建立一以前 TIP60 由调节在提供 Ran-GTP 水平的 homeostatic 控制的规章的机制运用了的 uncharacterized 为在有丝分裂的染色体分离的受动器绑定。 | Xiaoling Bao Heng Liu Xing Liu Ke Ruan Yonshui Zhang Zhiyong Zhang Qi Hu Ying Liu Saima Akram Jiahai Zhang Qingguo Gong Wenwen wang Xiao Yuan Jian-Li Lingli Zhao Zhen Dou Ruijun Tian Xuebiao Yao Jihui Wu Yunyu Shi | 2018 | Journal of Molecular Cell Biology2018，10，1： | 8 |
| 8 | Internalization of NK cells into tumor cells requires ezrin and leads to programmed cell-in-cell death显示文摘细胞毒素的淋巴细胞是在有缺点的房间的有免疫力的反应和消除的组织的关键播放器。我们以前报导了生来的杀手(NK ) 房间进入目标肿瘤房间,导致在肿瘤房间以内的任何一个目标房间死亡或自我毁灭。然而,它留下了至于在成为主观以后的 NK 房间的命运逃犯并且 heterotypic cell-in-cell 过程最近是否与同型的 cell-in-cell 事件的不同,说出 entosis。这里,我们证明 NK 房间在肿瘤房间以内与 apoptosis 的最终的命运经历一个 cell-in-cell 过程并且表明成为主观过程要求肌动朊细胞骨架管理者, ezrin。设想 NK 房间怎么进入肿瘤房间,我们执行了 NK 房间成为主观的即时双颜色成像分析进肿瘤房间。令人惊讶地,大多数 NK 房间在他们的入口以后承诺规划房间死亡进肿瘤房间,它与在同型的 cell-in-cell 过程观察的 entosis 区别地不同。使内在化的 NK 房间的 apoptotic 房间死亡由 caspase 的激活是明显的 3 并且 DNA 破碎。而且,在成为主观以后的 NK 房间死亡被 caspase 禁止者稀释, Z-VAD-FMK,在肿瘤房间以内作为 NK 房间死亡的模式证实 apoptosis。决定为 NK 房间的入口必要的蛋白质因素进肿瘤房间,我们执行了基于 siRNA 的击倒的分析并且在 NK 房间成为主观发现了 ezrin 的一个关键角色。重要地, ezrin 的调停 PKA 的 phosphorylation 支持 NK 房间成为主观过程。我们的调查结果建议 ezrin 由管理 NK 房间成为主观进肿瘤房间的新奇规章的机制。 | Shan Wang Zhen Guo Peng Xia Tingting Liu Jufang Wang Shan Li Lihua Sun Jianxin Lu Qian Wen Mingqian Zhou Li Ma Xia Ding Xiaoning Wang Xuebiao Yao | 2009 | Cell Research2009，19，12： | 6 |
| 9 | Allergic diseases, immunoglobulin E, and autoimmune pancreatitis: a retrospective study of 22 patients显示文摘 | Guo Limei Huang Yonghui Wang Tianli Shi Xueying Chang Hong Yao Wei Huang Xuebiao | 2014 | Chinese Medical Journal2014，，23： | 5 |
| 10 | Phosphorylation of human Sgo1 by NEK2A is essential for chromosome congression in mitosis显示文摘在有丝分裂的染色体分离被和锭子微导管的 thekinetochore 的相互作用安排。我们的最近的学习证明 NEK2A 在 thekinetochore 与 MAD1 交往并且可能作为锭子检查点发信号的一个新奇综合者工作。然而, NEK2A 怎么在有丝分裂调整 kinetochore 微导管附件,是不清楚的。这里,我们证明 thatNEK2A phosphorylates 人 Sgo1 和如此的磷酸化为在有丝分裂的忠诚 chromosomecongression 是必要的。NEK2A 直接绑在 HsSgo1 试管内并且与 HsSgo1 共同散布到有丝分裂的房间的 kinetochore。我们的试管内磷酸化实验表明了那 HsSgo1is NEK2A 和磷酸化地点的底层是由加入判定了被印射到重量的单位(14 ) 和重量的单位(507 )(32 ) P。尽管如此的磷酸化没为 HsSgo1to 的汇编被要求 kinetochore, non-phosphorylatable 异种 HsSgo1 的表示使不安 chromosomecongression 并且导致了微导管附件错误的戏剧的增加,包括 syntelicand monotelic 附件。这些调查结果在安排动态 kinetochore 微导管为调停 NEK2A 的 phosphorylationof HsSgo1 揭示一个关键角色相互作用。我们建议人的 Sgo1 的调停 thatNEK2A 的磷酸化在 kinetochores 提供在 centromeric 结合和锭子微导管附件之间的一个连接。 | Guosheng Fu Xia Ding Kai Yuan Felix Aikhionbare Jianhui Yao Xin Cai Kai Jiang Xuebiao Yao | 2007 | Cell Research2007，17，7： | 4 |
| 11 | Mitotic motor CENP-E cooperates with PRC1 in temporal control of central spindle assembly显示文摘Error-free cell division depends on the accurate assembly of the spindle midzone from dynamic spindle microtubules to ensure chromatid segregation during metaphase-anaphase transition.However,the mechanism underlying the key transition from the mitotic spindle to central spindle before anaphase onset remains elusive.Given the prevalence of chromosome instability phenotype in gastric tumorigenesis,we developed a strategy to model context-dependent cell division using a combination of light sheet microscope and 3D gastric organoids.Light sheet microscopic image analyses of 3D organoids showed that CENP-E inhibited cells undergoing aberrant metaphase-anaphase transition and exhibiting chromosome segregation errors during mitosis.Highresolution real-time imaging analyses of 2D cell culture revealed that CENP-E inhibited cells undergoing central spindle splitting and chromosome instability phenotype.Using biotinylated syntelin as an affinity matrix,we found that CENP-E forms a complex with PRC1 in mitotic cells.Chemical inhibition of CENP-E in metaphase by syntelin prevented accurate central spindle assembly by perturbing temporal assembly of PRC1 to the midzone.Thus,CENP-E-mediated PRC1 assembly to the central spindle constitutes a temporal switch to organize dynamic kinetochore microtubules into stable midzone arrays.These findings reveal a previously uncharacterized role of CENP-E in temporal control of central spindle assembly.Since CENP-E is absent from yeast,we reasoned that metazoans evolved an elaborate central spindle organization machinery to ensure accurate sister chromatid segregation during anaphase and cytokinesis. | Xu Liu Leilei Xu Junying Li Phil Y.Yao Wanjuan Wang Hazrat Ismail Haowei Wang Bryce Liao Zhihong Yang Tarsha Ward Ke Ruan Jianchun Zhang Quan Wu Ping He Xia Ding Dongmei Wang Chuanhai Fu Zhen Dou Feng Yan Wenwen Wang Xing Liu Xuebiao Yao | 2020 | Journal of Molecular Cell Biology2020，12，8： | 3 |
| 12 | Visualization and orchestration of the dynamic molecular society in cells显示文摘 | Xuebiao Yao Guowei Fang | 2009 | Cell Research2009，19，2： | 3 |
| 13 | Mitotic phosphorylation of PRC1 at Thr470 is required for PRC1 oligomerization and proper central spindle organization显示文摘在细胞分裂期间,染色体分离被和着丝点的锭子微导管的相互作用安排。进在分开的染色单体之间的一支组织中央锭子的 interpolarmicrotubules 的戏剧的改变为胞质分裂的开始和实行被要求。中央锭子组织要求有丝分裂的 kinesins, chromosomal 旅客蛋白质建筑群,和微导管捆绑蛋白质 PRC1。由在 Thr470 和 Thr481 的 Cdc2 的 PRC1 isphosphorylated 在有丝分裂期间。然而,在 Thr470 的功能的关联 ofPRC1 磷酸化留下了逃犯。这里,我们证明 thenon-phosphorylatable 异种 PRC1 (T470A ) 然而并非 phospho-mimicking 异种 PRC1 (T470E ) 的那表情引起中央锭子的异常组织。Immunoprecipitation 实验与野类型的 PRC1 显示那 bothPRC1 (T470A ) 和 PRC1 (T470E ) 突变蛋白质伙伴,建议 Thr470 的 thatphosphorylation 不改变 PRC1 自我协会。另外,在 vitroco 沉积,实验证明 PRC1 绑在独立于 Thr470 的 phosphorylationstate 的微导管。胶化过滤实验建议了 PRC1 的 Thr470 promotesoligomerization 的那磷酸化。给 Thr470 磷酸化的那预防禁止 PRC1oligomerization 试管内并且引起中央锭子体内的一个异常组织的事实,我们建议这 phosphorylation 依赖的 PRC1 oligomerization 保证中央锭子汇编在房间周期发生在适当时间。 | Chuanhai Fu Feng Yan Fang Wu Quan Wu Joseph Whittaker Haiying Hu Renming Hu Xuebiao Yao | 2007 | Cell Research2007，17，5： | 3 |
| 14 | Acetytation of ACAP4 regutates CCL18-elicited breast cancer cell migration and invasion显示文摘Tumor metastasis represents the main causes of cancer-related death.Our recent study showed that chemokine CCL18 secreted from tumor-associated macrophages regulates breast tumor metastasis,but the underlying mechanisms remain less clear.Here, we show that ARF6 GTPase-activating protein ACAP4 regulates CCL18-elicited breast cancer cell migration via the acetyltransferase PCAF-mediated acetylation.CCL18 stimulation elicited breast cancer cell migration and invasion via PCAF-dependent acetylation.ACAP4 physically interacts with PCAF and is a cognate substrate of PCAF during CCL18 stimulation.The acetylation site of ACAP4 by PCAF was mapped to Lys311 by mass spectrometric analyses.Importantly,dynamic acetylation of ACAP4 is essential for CCL18-induced breast cancer cell migration and invasion,as overexpression of the persistent acetylation-mimicking or nonacetylatable ACAP4 mutant blocked CCL18-elicited cell migration and invasion.Mechanistically,the acetylation of ACAP4 at Lys311 reduced the lipid-binding activity of ACAP4 to ensure a robust and dynamic cycling of ARF6-ACAP4 complex with plasma membrane in response to CCL18 stimulation.Thus,these results present a previously undefined mechanism by which CCL18-elicited acetylation of the PH domain controls dynamic interaction between ACAP4 and plasma membrane during breast cancer cell migration and invasion. | Xiaoyu Song Wei Liu Xiao Yuan Jiying Jiang Wanjuan Wang McKay Mullen Xuannv Zhao Yin Zhang Fusheng Liu Shihao Du Adeel Rehman Ruijun Tian Jian Li Andra Frost Zhenwei Song Hadiyah-Nicole Green Calmour Henry Xing Liu Xia Ding Dongmei Wang Xuebiao Yao | 2018 | Journal of Molecular Cell Biology2018，10，6： | 3 |
| 15 | SENP1 regulates IFN-γ-STAT1 signaling throug STAT3-SOCS3 negative feedback loop显示文摘干扰素 --(IFN-) 由激活发信号的细胞内部的 JAKSTAT1 为发炎反应触发巨噬细胞。表明 1 的 cytokine (SOCS1 ) 和蛋白质酷氨酸磷酸酶的 Suppressor 能否定地调制 IFN- 发信号。这里,我们鉴别一个新奇否定反馈环由 STAT3SOCS3 调停了,它被 SENP1 紧经由蛋白质酷氨酸磷酸酶 1B (PTP1B ) 的 de-SUMOylation 控制,在 IFN- 发信号。SENP1 缺乏的巨噬细胞在 IFN- 发信号和 M1 巨噬细胞激活显示出缺点。在 SENP1 缺乏的巨噬细胞的 PTP1B 高度 SUMOylated,它减少 STAT3 的导致 PTP1B 的 de-phosphorylation。激活的 STAT3 然后经由在 SENP1 缺乏的巨噬细胞感应的 SOCS3 压制 STAT1 激活。因此, SENP1 缺乏的巨噬细胞显示减少的能力抵抗 Listeria monocytogenes 感染。这些结果在巨噬细胞极化揭示控制 SENP1 的 STAT1 和 STAT3 平衡的一个关键角色。 | Tingting Yu Yong Zuo Rong Cai Xian Huang Shuai Wu Chenxi Zhang Y. Eugene Chin Dongdong Li Zhenning Zhang Nansong Xia Qi Wang Hao Shen Xuebiao Yao Zhong-Yin Zhang Song Xue Lei Shen Jinke Cheng | 2017 | Journal of Molecular Cell Biology2017，9，2： | 3 |
| 16 | Protein kinase TTK interacts and co-localizes with CENP-E to the kinetochore of human cells显示文摘Spindle checkpoint is an important biochemical signaling cascade during mitosis which monitors the fidelity of chromosome segregation, and is mediated by protein kinases Mpsl and Bubl/BubRl. Our recent studies show that kinesin-related motor protein CENP-E interacts with BubRl and participates in spindle checkpoint signaling. To elucidate the molecular mechanisms underlying spindle checkpoint signaling, we carried out proteomic dissection of human cell kinetochore and revealed protein kinase TTK, human homologue of yeast Mpsl. Our studies show that TTK is localized to the kinetochore of human cells, and interacts with CENP-E, suggesting that TTK may play an important role in chromosome segregation during mitosis. | Jie Zhang Chuanhai Fu Yong Miao Zhen Dou Xuebiao Yao | 2002 | Chinese Science Bulletin2002，47，23： | 3 |
| 17 | Emperipolesis, entosis and beyond: Dance with fate显示文摘 | Peng Xia Shan Wang Zhen Guo Xuebiao Yao | 2008 | Cell Research2008，18，7： | 3 |
| 18 | Chk1 prevents abnormal mitosis of S-phase HeLa cells containing DNA damage显示文摘To explore effects of DNA damage on cell-cycle progression in p53-deficient tumor cells, synchronized HeLa cells at G1, S and G2/M phases were treated with methyl methanesulfnate (MMS). The results showed that the MMS treatment resulted in the cell-cycle arrest or delay in all 3 phases, while the S-phase cells were the most sensitive to MMS. Further studies demonstrated that ATM-Chk2 and p38 MAPK signaling pathways were activated in all 3 phases when the cells were treated with MMS; whereas Chk1 was activated only in S phase under the drug treatment, indicating that Chk1 specifically participated in S-phase checkpoints. To analyze the role of Chk1 in S-phase checkpoints, we administered a specific Chk1 inhibitor, UCN-01, to the S-phase cells. The results showed that the S-phase cells treated with MMS+UCN-01 could enter aberrant mitosis without finishing DNA replication, indicating that Chk1 mainly functions in the DNA damage checkpoint rather than in the replication checkpoint. In addition, MMS treatment alone inhibited the accumulation of cyclin B1, a key component of M-phase CDK-cyclin complex, in the S-phase cells, whereas the inhibition of Chk1 activation resulted in the accumulation of cyclin B1 in the MMS-treated S-phase cells. This observation further supports the view that DNA-damaged S-phase cells enter abnormal mitosis when Chk1 activation is inhibited. Our results demonstrate that Chk1 is a specific kinase that plays an important role in the MMS-induced S-phase DNA damage checkpoint. As p53 is not involved in this process, Chk1 may be a potential target for p53-deficient tumor therapy. | LI XiaoFang WARD Tarsha YAO XueBiao WU JiaRui | 2009 | Chinese Science Bulletin2009，54，22： | 2 |
| 19 | Cyclin B1: conductor of mitotic symphony orchestra显示文摘被象染色体冷凝作用,面向双性人的锭子形成,染色体大会离子,分离和胞质分裂那样的一系列紧安排的事件精确通过有丝分裂调整。染色体运动被和位于着丝点以内的一个专业化染色体领域的锭子微导管的相互作用在有丝分裂期间管理。这个专业化区域,叫了 kinetochore,是为锭子微导管着丝点的地点协会。除了用作在染色体和锭子微导管之间的一个物理连接, kinetochore 通过微导管马达和定位在或在它附近的锭子集会检查点(囊) 传感器在 chromosomal 分离展出一个活跃角色[例如, 1 ] 。 | Huijuan Yu Xuebiao Yao | 2008 | Cell Research2008，18，2： | 2 |
| 20 | Functions of spindle check-point and its relationship to chromosome instability显示文摘It is generally believed that the equal distribution of genetic materials to two daughter cells during mitosis is the key to cell health and development. During the dynamic process, spindle checkpoint plays a very important role in chromosome movements and final sister chromatid separation. The equal and precise segregation of chromosomes contributes to the genomic stability while aberrant separations result in chromosome instability that causes pathogenesis of certain diseases such as Down’s syndrome and cancers. Kinetochore and its regulatory proteins consist of the spindle checkpoint and determine the spatial and temporal orders of chromosome segregation. | Jianhui Yao Yupeng Zheng Xuebiao Yao | 2002 | Chinese Science Bulletin2002，47，8： | 2 |
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