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| 1 | CKIP-1 regulates macrophage proliferation by inhibiting TRAF6-mediated Akt activation显示文摘巨噬细胞在开发,动态平衡,织物修理和免疫起枢轴的作用。巨噬细胞增长被刺激殖民地的因素(M-CSF ) 导致了 Akt 发信号的巨噬细胞支持;然而,这个过程怎么被终止,仍然保持不清楚。这里,我们作为巨噬细胞增长的一个新奇禁止者识别酷蛋白 kinase 2-interacting protein-1 (CKIP-1 ) 。在放松巨噬细胞, CKIP-1 是在由组成地活跃的 GSK3β 的丝氨酸 342 点的 phosphorylated;, Akt 的下游的目标。这 phosphorylation 触发 CKIP-1 的 polyubiquitination 和 proteasomal 降级。在 M-CSF 刺激之上, Akt 被 CSF-1R-PI3K 激活然后使 GSK3β 失去活性;,导致 CKIP-1 和 β 的稳定; -catenin 蛋白质。β -catenin 包括 cyclin D 和 c-Myc 支持增长基因的表示。CKIP-1 与 TRAF6,为连接 K63 的 ubiquitination 要求的 ubiquitin ligase 和 Akt 的血浆膜招募交往,并且终止调停 TRAF6 的 Akt 激活。由这个工具, CKIP-1 在 M-CSF 刺激以后在迟了的阶段明确地禁止巨噬细胞增长。而且, CKIP-1 缺乏在老鼠自发地开发的 vitro 和 CKIP-1 −/− 导致增加的增长和巨噬细胞的减少的 apoptosis 巨噬细胞主导的脾大和 myeloproliferation。一起,这些数据证明 CKIP-1 由禁止调停 TRAF6 的 Akt 激活在巨噬细胞动态平衡的规定起一个关键作用。 | Luo Zhang Yiwu Wang Fengjun Xiao Shaoxia Wang Guichun Xing Yang Li Xiushan Yin Kefeng Lu Rongfei Wei Jiao Fan Yuhan Chen Tao Li Ping Xie Lin Yuan Lei Song Lanzhi Ma Lujing Ding Fuchu He Lingqiang Zhang | 2014 | Cell Research2014，24，6： | 7 |
| 2 | CKIP-1 suppresses the adipogenesis of mesenchymal stem cells by enhancing HDACl-associated repression of C/EBPα显示文摘 | Dahu Li HengZhu Chao Liang Wenbo Li Guichun Xing Lanzhi Ma Lujing Ding Yi Zhang Fuchu He Lingqiang Zhang | 2014 | Journal of Molecular Cell Biology2014，8，5： | 4 |
| 3 | DNA damage stress induces the dissociation of Smurf1/2 from MDM2 in a slow manner显示文摘The tumor suppressor p53 locates at the key point of cell growth or apoptosis balance, and the expression level of p53 is tightly controlled by ubiquitin ligases including MDM2. Upon DNA damage stresses, p53 was accumulated and activated, leading to cell cycle arrest or apoptosis. We previously showed that Smad ubiquitylation regulatory factor 1/2 (Smurf1/2) promotes p53 degradation by interacting with and stabilizing MDM2, and consequently enhancing MDM2-mediated ubiquitylation of p53. However, it is unclear how the Smurf1-MDM2 interaction is regulated in response to DNA damage stress. Here, we show that in response to etoposide treatment Smurf1 dissociates from MDM2, resulting in MDM2 destabilization and p53 accumulation. The negative regulation of Smurf1 on apoptosis is released. Notably, this dissociation is a slow process rather than a rapid response, implicating high expression of Smurf1 might confer the resistance against p53 activation. Consistent with this notion, we observed that Smurf1/2 ligases are highly expressed in colon cancer, esophageal squamous cell carcinoma and pancreatic cancer tissues, suggesting the oncogenic tendency of Smurf1/2. | NIE Jing LIU Lin ZHAO XiaoHang XIE Ping ZHOU PingKun XING GuiChun LIU XiangJun HE FuChu HAN WeiDong ZHANG LingQiang | 2011 | Chinese Science Bulletin2011，56，30： | 2 |
| 4 | Differential regulation of Apak by various DNA damage signals显示文摘 | Shan Wang Chunyan Tian Tingtiang Xiao Guichun Xing Fuchu He Lingqiang Zhang Hong Chen | 2010 | Molecular and Cellular Biochemistry (-)2010，，1： | 1 |
| 5 | Characterization and expression of three novel differentiation-related genes belong to the human NDRG gene family显示文摘 | Xianghu Qu Yun Zhai Handong Wei Chenggang Zhang Guichun Xing Yongtao Yu Fuchu He | 2002 | Molecular and Cellular Biochemistry (-)2002，，1： | 1 |
| 6 | N-methylpurine DNA glycosylase inhibits p53-mediated cell cycle arrest and coordinates with p53 to determine sensitivity to alkylating agents显示文摘Alkylating 代理人导致染色体宽的基础损坏,它主要被 N-methylpurine DNA glycosylase (MPG ) 修理。因为导致 MPG 的 apurinic/apyrimidic (AP ) 地点触发更多的海滨裂缝,在肿瘤房间的某些类型的 MPG 的提高的表情授与更高的敏感到完化代理人。然而,药敏感或 insensitivity 的决定因素仍然保持不清楚。这里,我们报导 p53 地位与 MPG 协调在如此的过程起一个枢轴的作用。MPG 表示在胸,肺和结肠癌是积极的(38.7% , 43.4% 和 25.3% ,分别地) 但是在所有邻近的正常纸巾否定。MPG 直接绑在肿瘤 suppressor p53 并且镇压在不着重的房间的 p53 活动。而 MPG 的弄空增加了,减少的 MPG 的 overexpression,包括 p21 的 p53 下游的支持拘捕的基因的表示层次, 14-3-3 σ并且 Gadd45 然而并非 proapoptotic。MPG 的 N 终端区域明确地为和 p53 的 DNA 有约束力的域的相互作用被要求。在 DNA 完化应力之上,在 p53 野类型的肿瘤房间, p53 从 MPG 分裂了并且导致了房间生长拘捕。然后, AP 地点高效地被修理,它导致了 insensitivity 到 alkylating 代理人。由对比,在变异 p53 的房间, AP 地点与低功效被修理。到我们的知识,当 p53 的一个选择管理者,和这些调查结果在癌症治疗提供新卓见进在 MPG 和 p53 之间的功能的连接,这是第一条直接证据证明 DNA 修理酶功能。 | Shanshan Song Guichun Xing Lin Yuan Jian Wang Shan Wang Yuxin Yin Chunyan Tian Fuchu He Lingqiang Zhang | 2012 | Cell Research2012，22，8： | 1 |
| 7 | Differential regulation of Apak by various DNA damage signals显示文摘 | Shan Wang Chunyan Tian Tingtiang Xiao Guichun Xing Fuchu He Lingqiang Zhang Hong Chen | 2010 | Molecular and Cellular Biochemistry (-)2010，，1： | 1 |
| 8 | Ubiquitin ligase Smurf1 targets TRAF family proteins for ubiquitination and degradation显示文摘 | Shan Li Kefeng Lu Jian Wang Liguo An Guiwen Yang Hui Chen Yu Cui Xiushan Yin Ping Xie Guichun Xing Fuchu He Lingqiang Zhang | 2010 | Molecular and Cellular Biochemistry (-)2010，，1： | 1 |
| 9 | ARF-mediated SUMOylation of Apak antagonizes ubiquitylation and promotes its nucleolar accumulation to inhibit 47S pre-rRNA synthesis显示文摘Ribosomes are among the most fundamental molecular machines in all cells,as they are required for protein synthesis.Most structural rRNA components are generated in the nucleolus and assembled into pre-ribosomal particles.Here we show Apak,a previously identified p53 inhibitor,as a novel ribosomal stress response protein.In unstressed cells,Apak is bound to the deSUMOylase SENP1 in the nucleoplasm and targeted for proteasomal degradation by MDM2 ubiquitin ligase.Upon ribosomal stress,SENP1 dissociates fromApak and the tumor suppressor protein ARF couplesUbc9 with Apak to promote Apak SUMOylation on zinc fingers.This results in Apak protein stabilization and translocation to the nucleolus,where Apak inhibits the pre-rRNA synthesis.These findings provide a molecular mechanism whereby ARF coordinates Apak to regulate ribosome biogenesis upon cellular stress. | Shan Wang Siying Wang Lihua Yang Hua Guo Xue Kong Lin Yuan Guichun Xing Fuchu He Lingqiang Zhang | 2015 | Journal of Molecular Cell Biology2015，7，2： | 0 |
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