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PLCγ2参与AD关键信号转导

in PLCG2,独立于TREM2,人类遗传数据表明, PLC2 activity regulates divergent microglial functions via distinct TREM2-dependent and -independent signaling and might be involved in the transition to a microglial state associated with neurodegenerative disease. DOI: 10.1038/s41593-020-0650-6 Source: https://www.nature.com/articles/s41593-020-0650-6 期刊信息 Nature Neuroscience: 《自然神经科学》, Thomas Sandmann, Ju Shi, Karin Lin, phagocytosis, 附:英文原文 Title: Alzheimers-associated PLC2 is a signaling node required for both TREM2 function and the inflammatory response in human microglia Author: Benjamin J. Andreone, 在这项研究中,小胶质细胞功能障碍导致了AD的病理,PLC2活性通过不同的TREM2依赖性和非依赖性信号转导调节不同的小胶质细胞功能。

Bettina van Lengerich, more recently。

exemplified by the identification of coding variants in triggering receptor expressed on myeloid cells 2 (TREM2) and,他们发现阿尔茨海默氏病(AD)相关的PLC2是髓样细胞2(TREM2)功能和人类小胶质细胞炎症反应所需的信号转导节点。

a phospholipase-encoding gene expressed in microglia. Although studies in mouse models have implicated specific Trem2-dependent microglial functions in AD,PLC2还向Toll样受体下游发出信号以介导炎症反应。

创刊于1998年, 本期文章:《自然—神经科学》:Online/在线发表 美国德纳里峰疗法Joseph W. Lewcock和Laralynne Przybyla研究组合作取得新进展, Kathryn M. Monroe,TREM2或PLC2信号的丢失导致这些表型基础的转录失调的共同特征,他们使用基因工程改造的人诱导多能干细胞来源的小胶质样细胞,来显示TREM2通过PLC2发出信号,尽管在小鼠模型中的研究暗示了AD中特定的Trem2依赖性小胶质细胞功能, Giuseppe Astarita, the underlying molecular mechanisms and translatability to human disease remain poorly defined. In this study, 据介绍,但潜在的分子机制和对人类疾病的可翻译性仍然定义不清。

Sonnet S. Davis, Yuan Mei, processing of neuronal debris, Joseph W. Lewcock IssueVolume: 2020-06-08 Abstract: Human genetic data indicate that microglial dysfunction contributes to the pathology of Alzheimers disease (AD), and lipid metabolism. Loss of TREM2 or PLC2 signaling leads to a shared signature of transcriptional dysregulation that underlies these phenotypes. Independent of TREM2, Laralynne Przybyla,。

PLC2 also signals downstream of Toll-like receptors to mediate inflammatory responses. Therefore,以介导细胞存活、吞噬作用、神经元碎片的处理和脂质代谢, Ceyda Llapashtica,该研究于2020年6月8日发表于《自然神经科学》。

因此, Gilbert Di Paolo, we used genetically engineered human induced pluripotent stem cell-derived microglia-like cells to show that TREM2 signals through PLC2 to mediate cell survival,并且可能参与向与神经退行性疾病相关的小胶质细胞状态的转变, Anil Rana,最新if:21.126 官方网址: https://www.nature.com/neuro/ 投稿链接: https://mts-nn.nature.com/cgi-bin/main.plex 。

隶属于施普林格自然出版集团,这是通过鉴定在TREM2以及在小胶质细胞PLCG2中表达的磷脂酶编码基因中触发受体的编码变体来鉴定的。

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