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6篇 您的检索式:作者名="Ge Shaoyue"
    题名 作者 年代 出处 被引量
1The radial organization of neuronal primary cilia is acutely disrupted by seizure and ischemic brain injury显示文摘Neuronal 主要的睫是极其涉及中央神经系统(CNS ) 的合适的生长,发展,和功能的感觉细胞器。最近的工作也建议他们在 CNS 的上下文发信号损害,和那反常睫的发信号可以在神经病学的疾病被含有。我们确定了的方法 neuronal 的分发在整个由为主要的睫标记 adenylyl cyclase III (ACIII ) 染色并且关于全球、本地的并列飞机测量主要的睫的角度的 immunohistochemical 的正常成年老鼠大脑的主要的睫排列。我们然后介绍了尖锐大脑 insulttemporal 的二个不同模型脑叶抓住和服的局部缺血,和 re-examined neuronal 主要的睫分发,以及睫的长度和神经原怀有的比例睫。在基础条件下面的结果,外皮的睫关于外皮的表面放射状地排列自己,当时在有牙齿的回转的睫关于小粒房间层放射状地排列自己。在 striatum 和丘脑的神经原的睫由对比,展出睫的安排的宽分布。在尖锐大脑侮辱的两个盒子中,主要的睫排列显著地以一种区域特定的方式被破坏,与优先地破坏的侮辱影响的区域。进一步,二个模型在睫的长度上支持了微分效果,当仅仅局部缺血模型减少了时 ciliated 房间的比例。结论这些调查结果为 neuronal 的地区性的解剖组织提供证据在成年大脑的主要的睫并且建议各种各样的大脑侮辱可以破坏这个组织。Gregory W. Kirschen Hanxiao Liu Tracy Lang Xuelin Liang Shaoyu Ge Qiaojie Xiong 2017Frontiers in Biology2017,12,2:1
2A demand response and battery storage coordination algorithm for providing microgrid tie-line smoothing services显示文摘Wang Dan Ge Shaoyue Jia Hongjie 2014IEEE Transactions on Sustainable Energy2014,5,2:1
3Hypothalamic-Modified New Hippocampal Neurons for Alzheimer’s Disease显示文摘Alzheimer's disease(AD)is the leading cause of dementia worldwide.Although its pathology has been extensively studied,treatment options for AD remain limited.Any option to enhance the plasticity in the degenerating brain renders a potential treatment pathway for AD.Yan Gu Shaoyu Ge 2023Neuroscience Bulletin2023,39,11:0
4Centrosome positioning and primary cilia assembly orchestrate neuronal development显示文摘Sneha RAO Shaoyu GE Maya SHELLY 2012Frontiers of physics2012,7,5:0
5Adult hippocampal neurogenesis and its impairment in Alzheimer's disease显示文摘Adult neurogenesis is the creation of new neurons which integrate into the existing neural circuit of the adult brain.Recent evidence suggests that adult hippocampal neurogenesis(AHN)persists throughout life in mammals,including humans.These newborn neurons have been implicated to have a crucial role in brain functions such as learning and memory.Importantly,studies have also found that hippocampal neurogenesis is impaired in neurodegenerative and neuropsychiatric diseases.Alzheimer’s disease(AD)is one of the most common forms of dementia affecting millions of people.Cognitive dysfunction is a common symptom of AD patients and progressive memory loss has been attributed to the degeneration of the hippocampus.Therefore,there has been growing interest in identifying how hippocampal neurogenesis is affected in AD.However,the link between cognitive decline and changes in hippocampal neurogenesis in AD is poorly understood.In this review,we summarized the recent literature on AHN and its impairments in AD.Thomas A.Kim Michelle DSyty Kaitlyn Wu Shaoyu Ge 2022Zoological Research2022,43,3:0
6The deubiquitinating enzyme 13 retards non-alcoholic steatohepatitis via blocking inactive rhomboid protein 2-dependent pathway显示文摘Nowadays potential preclinical drugs for the treatment of nonalcoholic steatohepatitis(NASH)have failed to achieve expected therapeutic efficacy because the pathogenic mechanisms are underestimated.Inactive rhomboid protein 2(IRHOM2),a promising target for treatment of inflammation-related diseases,contributes to deregulated hepatocyte metabolism-associated nonalcoholic steatohepatitis(NASH)progression.However,the molecular mechanism underlying Irhom2 regulation is still not completely understood.In this work,we identify the ubiquitin-specific protease 13(USP13)as a critical and novel endogenous blocker of IRHOM2,and we also indicate that USP13 is an IRHOM2-interacting protein that catalyzes deubiquitination of Irhom2 in hepatocytes.Hepatocyte-specific loss of the Usp13 disrupts liver metabolic homeostasis,followed by glycometabolic disorder,lipid deposition,increased inflammation,and markedly promotes NASH development.Conversely,transgenic mice with Usp13 overexpression,lentivirus(LV)-or adeno-associated virus(AAV)-driven Usp13 gene therapeutics mitigates NASH in 3 models of rodent.Mechanistically,in response to metabolic stresses,USP13 directly interacts with IRHOM2 and removes its K63-linked ubiquitination induced by ubiquitin-conjugating enzyme E2N(UBC13),a ubiquitin E2 conjugating enzyme,and thus prevents its activation of downstream cascade pathway.USP13 is a potential treatment target for NASH therapy by targeting the Irhom2 signaling pathway.Minxuan Xu Jun Tan Liancai Zhu Chenxu Ge Wei Dong Xianling Dai Qin Kuang Shaoyu Zhong Lili Lai Chao Yi Qiang Li Deshuai Lou Linfeng Hu Xi Liu Gang Kuang Jing Luo Jing Feng Bochu Wang 2023Acta Pharmaceutica Sinica B2023,13,3:0
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