检索结果-南通市图书馆

Ecto-f_1-atpase: A moonlighting protein complex and an unexpected apoA-I receptor

World Journal of Gastroenterology 2010年第47期16卷 5925-5935页

作者： Pierre Vantourout Claudia Radojkovic Laeticia Lichtenstein Véronique Pons Eric Champagne Laurent O Martinez Institut national de la santé et de la recherche médicale U1048 Institute of Metabolic and Cardiovascular Diseases Université Toulouse III Paul-Sabatier

Mitochondrial atp synthase has been recently detected at the surface of different cell types, where it is a high affinity receptor for apoA-I, the major protein component in high density lipoproteins (HDL). Cell surface atp synthase (namely ecto-f1-atpase) expression is related to different biological effects, such as regulation of HDL uptake by hepatocytes, endothelial cell proliferation or antitumor activity of Vγ9/Vδ2 T lymphocytes. This paper reviews the recently discovered functions and regulations of ecto-f1-atpase. Particularly, the role of the f1-atpase pathway(s) in HDL-cholesterol uptake and apoA-Imediated endothelial protection suggests its potential importance in reverse cholesterol transport and its regulation might represent a potential therapeutic target for HDL-related therapy for cardiovascular diseases. Therefore, it is timely for us to better understand how this ecto-enzyme and downstream pathways are regulated and to develop pharmacologic interventions.

关键词： f1fo atp synthase High density lipoproteins receptor Apolipoprotein A-I Purinergic receptor P2Y13 Adenylate kinase Nucleotide Endothelium Antitumor immunity

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Oxidative stress battles neuronal Bcl-xL in a fight to the death

引用

Neural Regeneration Research 2021年第1期16卷 12-15页

作者： Han-A Park Katheryn Broman Elizabeth A.Jonas Department of Human Nutrition and Hospitality Management College of Human Environmental SciencesThe University of AlabamaTuscaloosaALUSA Department of Internal Medicine Section of EndocrinologyYale UniversityNew HavenCTUSA

Bcl-xL is a pro-survival protein of the Bcl2 family found in the mitochondrial ***-xL supports growth,development,and maturation of neurons,and it also prevents neuronal death during neurotoxic *** article reviews the mechanisms and upstream signaling that regulate the activity and abundance of *** team and others have reported that oxidative stress is a key regulator of intracellular Bcl-xL balance in *** stress regulates synthesis,degradation,and activity of Bcl-xL and therefore neuronal *** apoptosis,pro-apoptotic Bcl2 proteins such as Bax and Bak translocate to and oligomerize in the mitochondrial *** of oligomers causes release of cytochrome c and activation of caspases that lead to neuronal ***-xL binds directly to pro-apoptotic Bcl2 proteins to block apoptotic *** anti-apoptotic roles of Bcl-xL have been well documented,an increasing number of studies in recent decades show that protein binding partners of Bcl-xL are not limited to Bcl2 ***-xL forms a complex with f1fo atp synthase,DJ-1,DRP1,IP3R,and the ryanodine *** proteins support physiological processes in neurons such as growth and development and prevent neuronal damage by regulating mitochondrial atp production,synapse formation,synaptic vesicle recycling,neurotransmission,and calcium ***,under conditions of oxidative stress,Bcl-xL undergoes proteolytic cleavage thus lowering the abundance of functional Bcl-xL in ***,oxidative stress alters formation of Bcl-xL-mediated multiprotein complexes by regulating post-translational ***,oxidative stress regulates transcription factors that target the Bcl-x gene and alter accessibility of microRNA to mRNA influencing mRNA levels of *** this review,we discussed how Bcl-xL supports the normal physiology of neurons,and how oxidative stress contributes to pathology by manipulating the dynamics of Bcl

关键词： atp Bcl-xL f1fo atp synthase mitochondria neuroprotection oxidative stress

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：