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| 1 | Overexpression of SIRT3 disrupts mitochondrial proteostasis and cell cycle progression显示文摘 | Xiaofei Wang Haiping Tang Yuling Chen Binghuan Chi Shiyu Wang Yang Lv Di WU Renshan Ge Haiteng Deng | 2016 | Protein & Cell2016，7，4： | 3 |
| 2 | Calcium wave propagation in pancreatic acinar cells: functional interaction of inositol 1,4,5-trisphosphate receptors, ryanodine receptors, and mitochondria显示文摘 | STRAUB SV GIOVANNUCCI DR YULE DI | 2000 | J Gen Physiol2000，116，4： | 1 |
| 3 | Stimulant-evoked depolarization and increase ini in insulin-secreting cells is dependent on external Na+显示文摘 | Dunne MJ Yule DI Gallacher DV | 1990 | J Membr Biol1990，113，2： | 1 |
| 4 | Calcium and ~nitochondria显示文摘 | 3unter TE Yule DI Gunter KK | 2004 | FEBS Lett2004，567，1： | 1 |
| 5 | Tumor necrosis factor-alpha potentiates intraneuronal Ca2 + signaling via regulation of the inositol 1,4,5-trisphosphate receptor显示文摘 | Park KM Yule DI Bowers WJ | | 0，，48： | 1 |
| 6 | Ultrastructure and cell-cell coupling of cardiac myocytes differentiating in embryonic stem cell cuhures 显示文摘 | Westfall MV Pasyk KA Yule DI | 1997 | Cell Motil Cytoskeleton1997，36，1： | 1 |
| 7 | Detecting compromised email accounts via login behavior characterization显示文摘The illegal use of compromised email accounts by adversaries can have severe consequences for enterprises and society.Detecting compromised email accounts is more challenging than in the social network field,where email accounts have only a few interaction events(sending and receiving).To address the issue of insufficient features,we propose a novel approach to detecting compromised accounts by combining time zone differences and alternate logins to identify abnormal behavior.Based on this approach,we propose a compromised email account detection framework that relies on widely available and less sensitive login logs and does not require labels.Our framework characterizes login behaviors to identify logins that do not belong to the account owner and outputs a list of account-subnet pairs ranked by their likelihood of having abnormal login relationships.This approach reduces the number of account-subnet pairs that need to be investigated and provides a reference for investigation priority.Our evaluation demonstrates that our method can detect most email accounts that have been accessed by disclosed malicious IP addresses and outperforms similar research.Additionally,our framework has the capability to uncover undisclosed malicious IP addresses. | Jianjun Zhao Can Yang Di Wu Yaqin Cao Yuling Liu Xiang Cui Qixu Liu | 2024 | Cybersecurity2024，7，1： | 0 |
| 8 | Phosphorylation of Atg31 is required for autophagy显示文摘Autophagy 是降级的一个 evolutionarily 保存的细胞的过程细胞内部的内容。Atg17-Atg31-Atg29 建筑群在由各种各样的刺激感应的 autophagy 起一个关键作用。在酵母, autophagy 在说出的液泡附近在一个特殊地点与 autophagosome 形成发生 pre-autophagosomal 结构(舞步) 。Atg17-Atg31-Atg29 建筑群为舞步组织形成脚手架,并且招募其他人 autophagy 相关(Atg ) 蛋白质到 PAS。这里,我们证明 Atg31 是 phosphorylated 蛋白质。Atg31 上的 phosphorylation 地点被集体 spectrometry 识别。phosphorylated 氨基酸被丙氨酸在代替的异种的分析,个别地或在里面各种各样的联合,作为功能的 phosphorylation 地点识别了 S174。S174A 异种作为 Atg31 删除异种显示出 autophagy 缺陷的类似的度。S174 phosphorylation 为象氮饥饿和 rapamycin 处理那样的各种各样的 autophagy 刺激导致的 autophagy 被要求。集体 spectrometry 分析证明 S174 组成地是 phosphorylated,并且在 Atg31 删除紧张的 phosphorylation 模仿异种(S174D ) 的表示恢复 autophagy。在 S174A 异种, Atg9 积极的泡在 PAS 积累。因此, S174 phosphorylation 为 autophagosomes 的形成被要求,可能由便于从 PAS 再循环 Atg9。我们的数据在 autophagy 表明 Atg31 的 phosphorylation 的角色。 | Wenzhi Feng Tong Wu Xiaoyu Dan Yuling Chen Lin Li She Chen Di Miao Haiteng Deng Xinqi Gong Li Yu | 2015 | Protein & Cell2015，6，4： | 0 |
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