更新于：2024-11-01

ATP6V0C

更新于：2024-11-01

基本信息

别名

ATP6C、ATP6L、ATP6V0C

+ [12]

简介

Proton-conducting pore forming subunit of the V0 complex of vacuolar(H+)-ATPase (V-ATPase), a multisubunit enzyme composed of a peripheral complex (V1) that hydrolyzes ATP and a membrane integral complex (V0) that translocates protons (PubMed:33065002). V-ATPase is responsible for acidifying and maintaining the pH of intracellular compartments and in some cell types, is targeted to the plasma membrane, where it is responsible for acidifying the extracellular environment (By similarity).

关联

项与 ATP6V0C 相关的药物

Anti-VATPase nanobody(Tufts University)

靶点

ATP6V0C

作用机制

ATP6V0C blockers

在研机构

Tufts University

原研机构

Tufts University

在研适应症

乳腺癌

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 ATP6V0C 相关的临床结果

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100 项与 ATP6V0C 相关的转化医学

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0 项与 ATP6V0C 相关的专利（医药）

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170

项与 ATP6V0C 相关的文献（医药）

2024-10-01·Plant Physiology

FATTY ACID DESATURASE4 enhances plant RNA virus replication and undergoes host vacuolar ATPase-mediated degradation

Article

作者: Jia, Zhaoxing ; Rao, Shaofei ; Wu, Guanwei ; Yu, Tianqi ; Fang, Xinxin ; Rui, Penghuan ; Wu, Jian ; Lu, Yuwen ; Zheng, Hongying ; Yan, Fei ; Peng, Jiejun ; Chen, Jianping

AbstractEmerging evidence indicates that fatty acid (FA) metabolic pathways regulate host immunity to vertebrate viruses. However, information on FA signaling in plant virus infection remains elusive. In this study, we demonstrate the importance of fatty acid desaturase (FAD), an enzyme that catalyzes the rate-limiting step in the conversion of saturated FAs into unsaturated FAs, during infection by a plant RNA virus. We previously found that the rare Kua-ubiquitin-conjugating enzyme (Kua-UEV1) fusion protein FAD4 from Nicotiana benthamiana (NbFAD4) was downregulated upon turnip mosaic virus (TuMV) infection. We now demonstrate that NbFAD4 is unstable and is degraded as TuMV infection progresses. NbFAD4 is required for TuMV replication, as it interacts with TuMV replication protein 6K2 and colocalizes with viral replication complexes. Moreover, NbFAD4 overexpression dampened the accumulation of immunity-related phytohormones and FA metabolites, and its catalytic activity appears to be crucial for TuMV infection. Finally, a yeast 2-hybrid library screen identified the vacuolar H+-ATPase component ATP6V0C as involved in NbFAD4 degradation and further suppression of TuMV infection. This study reveals the intricate role of FAD4 in plant virus infection, and sheds light on a new mechanism by which a V-ATPase is involved in plant antiviral defense.

2024-09-01·Cortex

Functional integration and segregation during semantic cognition: Evidence across age groups

Article

作者: Wu, Wei ; Hoffman, Paul

Semantic cognition is underpinned by ventral anterior temporal lobe (vATL) which encodes knowledge representations and inferior frontal gyrus (IFG), which controls activation of knowledge based on the needs of the current context. This core semantic network has been validated in substantial empirical findings in the past. However, it remains unclear how these core semantic areas dynamically communicate with each other, and with other neural networks, to achieve successful semantic processing. Here, we investigated this question by testing functional connectivity in the core semantic network during semantic tasks and whether these connections were affected by cognitive ageing. Compared to a non-semantic task, semantic tasks increased the connectivity between left and right IFGs, indicating a bilateral semantic control system. Strengthened connectivity was also found between left IFG and left vATL, and this effect was stronger in the young group. At a whole-brain scale, IFG and vATL increased their coupling with multiple-demand regions during semantic tasks, even though these areas were deactivated relative to non-semantic tasks. This suggests that the domain-general executive network contributes to semantic processing. In contrast, IFG and vATL decreased their interaction with default mode network (DMN) areas during semantic tasks, even though these areas were positively activated by the task. This suggests that DMN areas do not contribute to all semantic tasks: their activation may sometimes reflect automatic retrieval of task-irrelevant memories and associations. Taken together, our study characterizes a dynamic connectivity mechanism supporting semantic cognition within and beyond core semantic regions.

2024-09-01·Cellular Signalling

Lysosomal dysfunction-derived autophagy impairment of gingival epithelial cells in diabetes-associated periodontitis with altered protein acetylation

Article

作者: Xie, Zhuo ; Li, Mengdi ; Huang, Xin ; Gao, Xianling ; Wei, Linhesheng ; Liu, Hui ; Lin, Zhengmei

Diabetes-associated periodontitis (DP) presents severe inflammation and resistance to periodontal conventional treatment, presenting a significant challenge in clinical management. In this study, we investigated the underlying mechanism driving the hyperinflammatory response in gingival epithelial cells (GECs) of DP patients. Our findings indicate that lysosomal dysfunction under high glucose conditions leads to the blockage of autophagy flux, exacerbating inflammatory response in GECs. Single-cell RNA sequencing and immunohistochemistry analyses of clinical gingival epithelia revealed dysregulation in the lysosome pathway characterized by reduced levels of lysosome-associated membrane glycoprotein 2 (LAMP2) and V-type proton ATPase 16 kDa proteolipid subunit c (ATP6V0C) in subjects with DP. In vitro stimulation of human gingival epithelial cells (HGECs) with a hyperglycemic microenvironment showed elevated release of proinflammatory cytokines, compromised lysosomal acidity and blocked autophagy. Moreover, HGECs with deficiency in ATP6V0C demonstrated impaired autophagy and heightened inflammatory response, mirroring the effects of high glucose stimulation. Proteomic analysis of acetylation modifications identified altered acetylation levels in 28 autophagy-lysosome pathway-related proteins and 37 sites in HGECs subjected to high glucose stimulation or siATP6V0C. Overall, our finding highlights the pivotal role of lysosome impairment in autophagy obstruction in DP and suggests a potential impact of altered acetylation of relevant proteins on the interplay between lysosome dysfunction and autophagy blockage. These insights may pave the way for the development of effective therapeutic strategies against DP.