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The E3 Ubiquitin Ligase gp78 Protects against ER Stress in Zebrafish Liver

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Journal of Genetics and Genomics 2014年第7期41卷 357-368页

作者： Zhiliang Chen Petek Ballar Yu Fu Jia Luo Shaojun Du shengyun fang Center for Biomedical Engineering and Technology Department of Physiology University of Maryland School of Medicine Faculty of Pharmacy Biochemistry DepartmentEge University Biopharmaceutical Research Institute Anhui Medical University Department of Internal Medicine University of Kentucky College of Medicine Department of Biochemistry and Molecular Biology University of Maryland School of Medicine

Enhanced endoplasmic reticulum （ER）-associated protein degradation （ERAD） activity by the unfolded protein response （UPR） represents one of the mechanisms for restoring ER homeostasis. In vitro evidence indicates that the mammalian gp78 protein is an E3 ubiquitin ligase that facilitates ERAD by polyubiquitinating and targeting proteins for proteasomal degradation under both physiologic and stress conditions. However, the in vivo function of gp78 in maintaining ER protein homeostasis remains untested. Here we show that like its mammalian counterpart, the zebrafish gp78 is also an E3 ubiquitin ligase as revealed by in vitro ubiquitination assays. Expression analysis uncovered that gp78 is highly expressed in several organs, including liver and brain, of both larval and adult fish. Treatment of larvae or adult fish with tunicamycin induces ER stress and upregulates the expression of several key components of the gp78 ERAD complex in the liver. Moreover, liver-specific overexpression of the dominant-negative form of gp78 （gp78-R2M） renders liver more sensitive to tunicamycin-induced ER stress and enhances the expression of sterol response element binding protein （Srebp）-target genes, which was largely suppressed in fish overexpressing wild-type gp78. Together, these data indicate that gp78 plays a critical role in protecting against ER stress in liver.

关键词： Zebrafish gp78/AMFR UPR Lipogenesis Cholesterol ERAD

Endoplasmic reticulum stress is involved in okadaic acid-induced tau phosphorylation and neurotoxic effects of okadaic acid

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Neural Regeneration Research 2010年第20期5卷 1534-1540页

作者： Lijie Feng Yuxian Shen Aimin Sun Yujun Shen shengyun fang Jun Li School of Pharmacy Anhui Medical University Hefei 230032 Anhui Province China Key Laboratory of Gene Resource Utilization for Genetic Diseases of Educational Ministry and Anhui Province Anhui Medical University Hefei 230032 Anhui Province China Institute of Medical and Pharmaceutical Biotechnology Anhui Medical University Hefei 230032 Anhui Province China

The role of the endoplasmic reticulum in Alzheimer＇s disease pathogenesis remains poody understood.The present study investigated the correlation of okadaic acid-induced tau hyperphosphorylation and neurotoxicity with endoplasmic reticulum stress.Following co-culture of various concentrations of okadaic acid （25,50,100,and 200 nmol/L） and human neuroblastoma SH-SY5Y cells,okadaic acid,a selective protein phosphatase （PP-1,PP-2A） inhibitor,reduced cell viability in a concentration-dependent manner,which was closely associated with okadaic acid-induced tau phosphorylation.In addition,expressions of the unfolded protein response activation marker glucose-regulated protein 78 （BiP/Grp78） and the CCAAT/enhancer binding protein homologous protein （CHOP）/Gadd153 increased following okadaic acid treatment.Furthermore,the unfolded protein response was activated in human embryonic kidney 293 （HEK 293） cells overexpressing tau following okadaic acid treatment,but untransfected HEK 293 cells did not exhibit activation of the unfolded protein response.These data indicate that endoplasmic reticulum stress is involved in mechanisms underlying tau phosphorylation and the cytotoxic effects of okadaic acid.

关键词： tau phosphorylation endoplasmic reticulum stress unfolded protein response

BAF45D cooperates with SMAD signaling and promotes early neural differentiation in P19 and H9 cells

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BAF45D cooperates with SMAD signaling and promotes early neu...

BAF45D cooperates with SMAD signaling and promotes early neural differentiation in P19 and H9 cells

中国解剖学会2021年年会

作者： Hu Xiujuan Jiang Jing Chen Xueying Liu Chang Liu Lihua fang shengyun Shen Yuxian Liu Chao Department of Histology and Embryology Institute of Stem Cell and Tissue EngineeringSchool of Basic Medical Sciences Institute of Clinical Pharmacology Anhui Medical University Center for Biomedical Engineering and Technology University of Maryland

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解剖学杂志 2021年第S1期44卷 220-220页

作者： Hu Xiujuan Jiang Jing Chen Xueying Liu Chang Liu Lihua fang shengyun Shen Yuxian Liu Chao Department of Histology and Embryology Institute of Stem Cell and Tissue EngineeringSchool of Basic Medical Sciences Institute of Clinical Phar macology Anhui Medical UniversityHefei 230032 Center for Biomedical Engineering and Technology University of MarylandBaltimoreMD 21201USA

BAF45Dis a member of BAF complex,which may play a crucial role in neural development.PAX6 determines neuroectoderm formation,which is highly level sensitive.BAF45D is required for retinoic acid(RA)induced PAX6 expression.PAX6 expression is also regulated by TGF-beta/SMAD signaling.However,mechanism of such regulation remains elusive.We therefore sought to explore whether BAF45D regulates PAX6 expression through cooperating with TGF-beta/SMAD signaling.Here we identified BAF45D is required for expression of phosphorylated SMAD3 and PAX6 induced by RA.Genome-wide analysis revealed that during RA-induced early neural differentiation,BAF 45D knockdown failed to activate TGF-beta/SMAD signaling and induce expression of STAT3 and SMAD7,two negative regulators of TGF-beta/SMAD signaling.Moreover,in RA treated P19 and H9 cells,BAF45D interacts with BRG1 and phosphorylated SMAD3.

关键词： SMAD expression. PAX6

ER membrane ubiquitin ligase Hrdl mediates tau degradation in proteosome-dependent and independent manner

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中国药理通讯 2007年第2期24卷 39-40页

作者： Lijie Feng Yuxian Shen shengyun fang Hailong Hou Hui fang Haiping Wang Jiangning Zhou Institute of Clinical Pharmacology Anhui Medical University Hefei China Department of Neurobiology School of Life Science University of Science and Technology of China Hefei China Medical Biotechnology Center University of Maryland Biotechnology Institute Baltimore MD USA

Abnormal accumulation of hyperphosphorylated tau protein in intracellular inclusions is a recognized pathological feature in a number of dementias, which is collectively called tauopathies. To explore the molecular mechanism by which tauopthies are regulated, we investigated the effects of human Hrdl, an endoplasmic reticulum (ER) membrane ubiquitin ligase (E3) with RING finger domain,

关键词：蛋白酶老年性痴呆降解能力神经元

ER membrane ubiquitin ligase Hrdl normally expressed is required for neuron survival in Alzheimer＇s disease

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中国药理通讯 2007年第2期24卷 40-41页

作者： Yuxian Shen Lijie Feng shengyun fang Hailong Hou Qi Li Haiping Wang Hui fang Jiangning Zhou Hefei National Laboratory for Physical Sciences at Microscale and Departmentof Neurobiology and Biophysics School of Life Science Universityof Science and Technology of China Hefei China Institute of Clinical Pharmacology Anhui Medical University Hefei China Medical Biotechnology Center University of Maryland Biotechnology Institute Baltimore MD USA

Neurofibrillary tangles (NFTs) are the most common intraneuronal inclusion in the brains of patients with neurodegenerative diseases and have been implicated in mediating neuronal death and cognitive deficits. Here, we found that an integral ER membrane ubiquitin ligase (E3) Hrdl expresses extensively in the hippocampal neurons and colocalizes with Alz50,

关键词：阿尔茨海默病神经元患者痴呆症

DPF2 interacts with and regulates Oct4 protein level and localization

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DPF2 interacts with and regulates Oct4 protein level and loc...

Ubiquitin ligase gp78 increases solubility and facilitates degradation of the Z variant of α- 1 -antitrypsin

中国解剖学会2015年年会

作者： Chao Liu Dijuan Zhang Lihua Liu shengyun fang Department of Histology and Embryology Anhui Medical University Center for BioMET University of Maryland

＜正＞A tight regulation of Oct4 levels plays a crucial role in mammalian embryonic development and oncogenesis.However,the mechanisms underlying regulation of Oct4 protein level are largely unknown.Here,we report that DPF2,a PHD-domain containing protein,is upregulated during H9 cell differentiation induced by retinoic acid.Endogenous interaction between DPF2

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中国药理通讯 2006年第3期23卷 40-40页

作者： Yuxian Shen Petek Ballar shengyun fang Medical Bioteehnology Center University of Maryland Bioteehnology Institute Baltimore MD 21201 USA Institute of Clinical Pharmacology Anhui Medical University Hefei 230032 China

α- 1 - antitrypsin (AAT) is the most abundant circulating serine proteinase inhibitor of the serpin superfamily。Deficiency of circulating AAT is the most widely recognized abnormality of a proteinase inhibitor that causes lung disease。AAT deficiency is caused by mutations of the AAT gene that lead to AAT protein retention in the endoplasmic reticulum (ER)。Moreover, the mutant AAT accumulated in the ER predisposes the homozygote to severe liver injuries, such as neonatal hepatitis, juvenile cirrhosis, and hepatocellular carcinoma。Despite the fact that mutant AAT protein is subject to Erassociated degradation we report that gp78, a ubiquitin ligase (E3) pairing with mammalian Ubc7 for ERAD, ubiquitinates and facilitates degradation of ATZ。the classic deficiency variant of AAT having a Z mutation (Glu342Lys)。

关键词：泛激素连接酶溶解度 α-1-抗胰蛋白酶生物化学

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基于行人组运动信息表达的人群异常检测

仪器仪表学报 2022年第6期43卷 221-229页

作者：周生运张旭光方银锋杭州电子科技大学通信工程学院杭州310018

人群异常检测是智能化人群监控技术下的一个重要研究方向,在现有的方法中,异常检测的首要步骤就是获取运动信息,传统通过对视频帧均匀分块的方式并不能保证行人的完整性,提取的特征也不能准确反映行人的运动状态。本文提出了递进式人群... 详细信息

人群异常检测是智能化人群监控技术下的一个重要研究方向,在现有的方法中,异常检测的首要步骤就是获取运动信息,传统通过对视频帧均匀分块的方式并不能保证行人的完整性,提取的特征也不能准确反映行人的运动状态。本文提出了递进式人群分组的方法,先将人群运动场与帧差法结合分割图像获取人群前景,然后依据人群运动方向获取方向组,结合时空信息对方向组再聚类,得到更细致的行人组。对于每个行人组,利用人群能量特征去表征行人整体运动信息,并依据能量场构造了环块能量直方图特征来削弱行人四肢摆动的影响,最后与图像外观特征相结合用于人群异常检测。实验结果表明,本文方法在两个不同场景下帧级准确率达到83%和92%,像素级准确率达到64%和83%,与传统方法相比有较大提升。

关键词：人群监控人群异常检测运动信息行人组环块能量直方图