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| 1 | Characteristics of atmospheric single particles during haze periods in a typical urban area of Beijing:A case study in October,2014显示文摘To investigate the composition and possible sources of particles, especially during heavy haze pollution, a single particle aerosol mass spectrometer(SPAMS) was deployed to measure the changes of single particle species and sizes during October of 2014, in Beijing. A total of 2,871,431 particles with both positive and negative spectra were collected and characterized in combination with the adaptive resonance theory neural network algorithm(ART-2a). Eight types of particles were classified: dust particles(dust, 8.1%), elemental carbon(EC, 29.0%), organic carbon(OC, 18.0%), EC and OC combined particles(ECOC, 9.5%),Na-K containing particles(Na K, 7.9%), K-containing particles(K, 21.8%), organic nitrogen and potassium containing particles(KCN, 2.3%), and metal-containing particles(metal,3.6%). Three haze pollution events(P1, P2, P3) and one clean period(clean) were analyzed,based on the mass and number concentration of PM_(2.5)and the back trajectory results from the hybrid single particle Lagrangian integrated trajectory model(Hysplit-4 model). Results showed that EC, OC and K were the major components of single particles during the three haze pollution periods, which showed clearly increased ratios compared with those in the clean period. Results from the mixing state of secondary species of different types of particles showed that sulfate and nitrate were more readily mixed with carbon-containing particles during haze pollution episodes than in clean periods. | Lang Liu Yanli Wang Shiyong Du Wenjie Zhang Lujian Hou Sverre Vedal Bin Han Wen Yang Mindong Chen Zhipeng Bai | 2016 | Journal of Environmental Sciences2016，28，2： | 19 |
| 2 | Ubiquitination of Rheb governs growth factor-induced mTORC1 activation显示文摘Mechanistic target of rapamycin mTOR complex 1 (mTORC1)plays a key role in the integration of various environmental signals to regulate cell growth and metabolism,mTORC1 is recruited to the lysosome where it is activated by its interaction with GTP-bound Rheb GTPase.However,the regulatory mechanism of Rheb activity remains largely unknown.Here,we show that ubiquitination governs the nucleotide-bound status of Rheb.Lysosome-anchored E3 ligase RNF152 catalyzes Rheb ubiquitination and promotes its binding to the TSC complex.EGF enhances the deubiquitination of Rheb through AKT-dependent USP4 phosphorylation,leading to the release of Rheb from the TSC complex.Functionally,ubiquitination of Rheb is linked to mTORC1-mediated signaling and consequently regulates tumor growth.Thus,we propose a mechanistic model whereby Rheb-mediated mTORC1 activation is dictated by a dynamic opposing act between Rheb ubiquitination and deubiquitination that are catalyzed by RNF152 and USP4 respectively. | Lu Deng Lei Chen Linlin Zhao Yan Xu Xiaoping Peng Xinbo Wang Lin Ding Jiali Jin Hongqi Teng Yanming Wang Weijuan Pan Fei Yu Lujian Liao Li Li Xin Ge Ping Wang | 2019 | Cell Research2019，29，2： | 16 |
| 3 | Induction of Wnt signaling antagonists and p21-activated kinase enhances cardiomyocyte proliferation during zebrafish heart regeneration显示文摘Heart regeneration occurs by dedifferentiation and proliferation of pre-existing cardiomyocytes(CMs).However,the signaling mechanisms by which injury induces CM renewal remain incompletely understood.Here,we find that cardiac injury in zebrafish induces expression of the secreted Wnt inhibitors,including Dickkopf 1(Dkkl),Dkk3,secreted Frizzled-related protein 1(sFrpl),and sFrp2,in cardiac tissue adjacent to injury sites.Experimental blocking of Wnt activity via Dkkl overexpression enhances CM proliferation and heart regeneration,whereas ectopic activation of Wnt8 signaling blunts injury-induced CM dedifferentiation and proliferation.Although Wnt signaling is dampened upon injury,the cytoplasmic β-catenin is unexpectedly increased at disarrayed CM sarcomeres in myocardial wound edges.Our analyses indicated that p21-activated kinase 2(Pak2)is induced at regenerating CMs,where it phosphorylates cytoplasmic β-catenin at Ser 675 and increases its stability at disassembled sarcomeres.Myocardial-specific induction of the phospho-mimeticβ-catenin(S675E)enhances CM dedifferentiation and sarcomere disassembly in response to injury.Conversely,inactivation of Pak2 kinase activity reduces the Ser 675-phosphorylatedβ-catenin(pS675-β-catenin)and attenuates CM sarcomere disorganization and dedifferentiation・Taken together,these findings demonstrate that coordination of Wnt signaling inhibition and Pak2/pS675-βYatenin signaling enhances zebrafish heart regeneration by supporting CM dedifferentiation and proliferation. | Xiangwen Peng Kaa Seng Lai Peilu She Junsu Kang Tingting Wang Guobao Li Yating Zhou jianjian Sun Daqing Jin Xiaolei Xu Lujian Liao Jiandong Liu Ethan Lee Kenneth D.Poss Tao P.Zhong | 2021 | Journal of Molecular Cell Biology2021，13，1： | 3 |
| 4 | PINK1 kinase dysfunction triggers neurodegeneration in the primate brain without impacting mitochondrial homeostasis显示文摘In vitro studies have established the prevalent theory that the mitochondrial kinase PINK1 protects neurodegeneration by removing damaged mitochondria in Parkinson's disease(PD).However,difficulty in detecting endogenous PINK1 protein in rodent brains and cell lines has prevented the rigorous investigation of the in vivo role of PINK1.Here we report that PINK1 kinase form is selectively expressed in the human and monkey brains.CRISPR/Cas9-mediated deficiency of PINK1 causes similar neurodegeneration in the brains of fetal and adult monkeys as well as cultured monkey neurons without affecting mitochondrial protein expression and morphology.Importantly,PINK1 mutations in the primate brain and human cells reduce protein phosphorylation that is important for neuronal function and survival.Our findings suggest that PINK1 kinase activity rather than its mitochondrial function is essential for the neuronal survival in the primate brains and that its kinase dysfunction could be involved in the pathogenesis of PD. | Weili Yang Xiangyu Guo Zhuchi Tu Xiusheng Chen Rui Han Yanting Liu Sen Yan Qi Wang Zhifu Wang Xianxian Zhao Yunpeng Zhang Xin Xiong Huiming Yang Peng Yin Huida Wan Xingxing Chen Jifeng Guo Xiao-Xin Yan Lujian Liao Shihua Li Xiao-Jiang Li | 2022 | Protein & Cell2022，13，1： | 3 |
| 5 | Nuclear UHRF1 is a gate-keeper of cellular AMPK activity and function显示文摘The AMP-activated protein kinase(AMPK)is a central regulator of energy homeostasis.Although much has been learned on how low energy status and glucose starvation activate AMPK,how AMPK activity is properly controlled in vivo is still poorly understood.Here we report that UHRF1,an epigenetic regulator highly expressed in proliferating and cancer cells,interacts with AMPK and serves to suppress AMPK activity under both basal and stressed conditions.As a nuclear protein,UHRF1 promotes AMPK nuclear retention and strongly suppresses nuclear AMPK activity toward substrates H2B and EZH2.Importantly,we demonstrate that UHRF1 also robustly inhibits AMPK activity in the cytoplasm compartment,most likely as a consequence of AMPK nucleocytoplasmic shuttling.Mechanistically,we found that UHRF1 has no obvious effect on AMPK activation by upstream kinases LKB1 and CAMKK2 but inhibits AMPK activity by acting as a bridging factor targeting phosphatase PP2A to dephosphorylate AMPK.Hepatic overexpression of UHRF1 showed profound effects on glucose and lipid metabolism in wild-type mice but not in those with the liver-specific knockout of AMPKα1/α2,whereas knockdown of UHRF1 in adipose tissue led to AMPK activation and reduced sizes of adipocytes and lipogenic activity,highlighting the physiological significance of this regulation in glucose and lipid metabolism.Thus,our study identifies UHRF1 as a novel AMPK gate-keeper with critical roles in cellular metabolism. | Xiang Xu Guangjin Ding Caizhi Liu Yuhan Ding Xiaoxin Chen Xiaoli Huang Chen-Song Zhang Shanxin Lu Yunpeng Zhang Yuanyong Huang Zhaosu Chen Wei Wei Lujian Liao Shu-Hai Lin Jingya Li Wei Liu Jiwen Li Sheng-Cai Lin Xinran Ma Jiemin Wong | 2022 | Cell Research2022，32，1： | 3 |
| 6 | Baf60b-mediated ATM-p53 activation blocks cell identity conversion by sensing chromatin opening显示文摘由系特定的抄写因素的表示的系变换是改变那的 epigenetic 的进程有低效率。一个房间由抵抗系变换的机制大部分是未知的。使用肝特定的抄写因素 Foxa3, Hnf1 和 Gata4 (3TF ) 在老鼠成纤维细胞导致肝的变换,我们证明 3TF 导致了 ATM-p53 小径的强壮的激活,它导致了增长拘捕和房间死亡,和它进一步阻止了肝的变换。尤其是, ATM 激活,独立于 DNA 损坏,对染色质在肝的变换期间开作出回应。由在肝的变换期间描绘早分子的事件,我们发现了那 Baf60b,改变建筑群的 SWI/SNF 染色质的一个成员,连接染色质洞到由便于 ATM 招募到肝的基因 loci 的一块面板的开的染色质区域的 ATM 激活。这些调查结果由在察觉到揭示 ATM-p53 小径的功能使细胞的回答清楚些到系变换染色质洞。 | Shuyi Ji Linying Zhu Yimeng Gao Xiaoran Zhang Yupeng Yan Jin Cen Rongxia Li Rong Zeng Lujian Liao Chunhui Hou Yawei Gao Shaorong Gao Gang Wei Lijian Hui | 2017 | Cell Research2017，27，5： | 2 |
| 7 | In Situ Synthesis of Nanocrystalline Intermetallic Compound Layer during Surface Mechanical Attrition Treatment of Zirconium显示文摘The surface mechanical attrition treatment (SMAT) technique was developed to synthesize a nanocrystalline (NC) layer on the surface of metallic materials for upgrading their overall properties and performance. In this paper, by means of SMAT to a pure zirconium plate at the room temperature, repetitive multidirectional peening of steel shots (composition (wt%): 1C, l.SCr, base Fe) severely deformed the surface layer. A NC surface layer consisting of the intermetallic compound FeCr was fabricated on the surface of the zirconium. The microstructure characterization of the surface layer was performed by using X-ray diffraction analysis, optical microscopy, scanning and transmission electron microscopy observations. The NC surface layer was about 25 urn thick and consisted of the intermetallic compound FeCr with an average grain size of 25±10 nm. The deformation-induced fast diffusion of Fe and Cr from the steel shots into Zr occurred during SMAT, leading to the formation of intermetallic compound. In addition, the NC surface layer exhibited an ultrahigh nanohardness of 10.2 GPa. | SUNCai-yun XIEJi-jia WUXiao-lei HONGYou-shi LIUGang LUJian LUKe | 2004 | 材料热处理学报2004，25，05B： | 2 |
| 8 | Prostate cancer detection is also relevant in low prostate specific antigen range显示文摘 | Lujian M Paez A Miravalles E | 2004 | Eur Urol2004，45，2： | 1 |
| 9 | The Intracellular Cargo Receptor ERGIC-53 Is Required for the Production of Infectious Arenavirus, Coronavirus, and Filovirus Particles显示文摘 | Joseph P. Klaus Philip Eisenhauer Joanne Russo Anne B. Mason Danh Do Benjamin King Douglas Taatjes Cromwell Cornillez-Ty Jonathan E. Boyson Markus Thali Chunlei Zheng Lujian Liao John R. Yates Bin Zhang Bryan A. Ballif Jason W. Botten | 2013 | Cell Host & Microbe2013，，5： | 1 |
| 10 | Intensity-modu-lated whole pelvic rdiotherapy in women withgynecologicmalignancies显示文摘 | Mundt AJ lujian AE Rotmensch J | 2002 | Int J Radiat Oncol BiolPhys2002，52，5： | 1 |
| 11 | Intensity-modulated whole pelvic radiation therapy in patients with gynecologic malignancies显示文摘 | Roeske J C Lujian A Rotmensch J | 2000 | Int J Radiat Oncol Biol Phys2000，48，5： | 1 |
| 12 | Intensity modulated whole pelvic radiation therapy in patients with gynecological malignancies显示文摘 | LUJIAN A ROTMENSCH J | 2000 | Int J Radial Oncol Biol Phys2000，48，： | 1 |
| 13 | Long term survival after laparoscopic colon resection for cancer:complete five-year follow-up显示文摘 | Lujian HJ Pasencia G Jacobs M | 2002 | Dis Colon Rectum2002，45，4： | 1 |
| 14 | 显示文摘 | FengGan(冯淦) ShiLianjie(石连捷) LuJian(吕坚)etal | 2000 | 金属学报2000，3，36： | 1 |
| 15 | Synthesis and nonlinear optical properties of a series of azo chromophore functionalized alkox- ysilanes显示文摘 | Cui Yuanjing Qian Guodong Chen Lujian | 2008 | Dyes and Pigments2008，77，1： | 1 |
| 16 | Intensity-modula- ted whole pelvic radiotherapy in women with gynecologic ma- lignancies显示文摘 | Mundt AJ Lujian AE Rotmensch J | 2002 | Int J Radiat Oncol Bio Phys2002，52，5： | 1 |
| 17 | 1 CaMKII in lateral habenuia mediates core symptoms of depression 显示文摘 | Kun Li Tao Zhou Lujian Liao et aI | 2013 | Sci-ence2013，6149，341： | 1 |
| 18 | Second-order nonlinear optical properties of cross-linked silica films prepared through sol-gel process显示文摘 | Cui Yuanjing Qian Guodong Chen Lujian | 2008 | Thin Solid Films2008，516，： | 1 |
| 19 | Laparoscopic cholecystectomy vs open cholecystectomy in the treatment of acute cholecystitis: a prospective study显示文摘 | Lujian JA Parrilla P Robles R | 1998 | Arch Surg1998，133，2： | 1 |
| 20 | Variantspecific surface protein switching in Giardia lambli显示文摘 | NASH TE LUJIAN HD MOWATT MR | 2001 | Infec Immun2001，69，： | 1 |
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