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FAM19A5是一种脂肪因子吗?野生型、FAM19A5基因敲除型和LacZ基因敲入型小鼠的外周FAM19A5 。

Is FAM19A5 an adipokine? Peripheral FAM19A5 in wild-type, FAM19A5 knockout, and LacZ knockin mice.

作者信息

Kwak Hoyun, Cho Eun-Ho, Cho Eun Bee, Lee Yoo-Na, Shahapal Anu, Yong Hyo Jeong, Reyes-Alcaraz Arfaxad, Jeong Yongwoo, Lee Yerim, Lee Minhyeok, Ha Nui, Oh Sitaek, Lee Jae Keun, Lee Won Suk, Kim Won Kyum, Yoo Sangjin, Kwon Soon-Gu, Hwang Jong-Ik, Seong Jae Young

机构信息

Neuracle Science Co., Ltd., Seoul 02841, Republic of Korea.

Department of Biomedical Sciences, Graduate School of Medicine, Korea University, Seoul 02841, Republic of Korea.

出版信息

Mol Cells. 2024 Dec;47(12):100125. doi: 10.1016/j.mocell.2024.100125. Epub 2024 Oct 18.

DOI:10.1016/j.mocell.2024.100125
PMID:39426682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11603079/
Abstract

FAM19A5 is a novel secretory protein expressed primarily in the brain. However, a recent study reported that FAM19A5 is an adipocyte-derived adipokine that regulates vascular smooth muscle function through sphingosine-1-phosphate receptor 2 (S1PR2). In our study, we investigated FAM19A5 transcript and protein levels in peripheral tissues, including adipose tissues, from wild-type, FAM19A5 knockout, and FAM19A5-LacZ knockin mice. We found that the FAM19A5 transcript levels in the central nervous system were much greater than those in any of the peripheral tissues, including adipose tissues. Furthermore, the FAM19A5 protein levels in adipose and reproductive tissues were below detectable limits for Western blot analysis and enzyme-linked immunosorbent assay (ELISA). Additionally, we found that the FAM19A5 protein did not interact with S1PR2 in terms of G-protein-mediated signal transduction, β-arrestin recruitment, or ligand-mediated internalization. Taken together, our findings revealed basal levels of FAM19A5 transcripts and proteins in peripheral tissues, confirming its primary expression in the central nervous system and lack of significant interaction with S1PR2.

摘要

FAM19A5是一种主要在大脑中表达的新型分泌蛋白。然而,最近一项研究报道称,FAM19A5是一种源自脂肪细胞的脂肪因子,它通过1-磷酸鞘氨醇受体2(S1PR2)调节血管平滑肌功能。在我们的研究中,我们调查了野生型、FAM19A5基因敲除型和FAM19A5-LacZ基因敲入型小鼠外周组织(包括脂肪组织)中的FAM19A5转录本和蛋白水平。我们发现,中枢神经系统中的FAM19A5转录本水平远高于包括脂肪组织在内的任何外周组织。此外,脂肪组织和生殖组织中的FAM19A5蛋白水平低于蛋白质印迹分析和酶联免疫吸附测定(ELISA)的可检测限。此外,我们发现,在G蛋白介导的信号转导、β-抑制蛋白募集或配体介导的内化方面,FAM19A5蛋白与S1PR2没有相互作用。综上所述,我们的研究结果揭示了外周组织中FAM19A5转录本和蛋白的基础水平,证实了其在中枢神经系统中的主要表达以及与S1PR2缺乏显著相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/bd7a48145833/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/d058f4f41e58/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/33ef05c2fa34/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/07c3619a6775/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/37f0b45876f4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/bd7a48145833/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/d058f4f41e58/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/33ef05c2fa34/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/07c3619a6775/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/37f0b45876f4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed92/11603079/bd7a48145833/gr5.jpg

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引用本文的文献

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Partial FAM19A5 deficiency in mice leads to disrupted spine maturation, hyperactivity, and an altered fear response.小鼠中FAM19A5部分缺陷会导致脊柱成熟受阻、多动以及恐惧反应改变。
PLoS One. 2025 Aug 5;20(8):e0327493. doi: 10.1371/journal.pone.0327493. eCollection 2025.
2
Inhibition of FAM19A5 reverses synaptic loss and cognitive decline in mouse models of Alzheimer's disease.抑制FAM19A5可逆转阿尔茨海默病小鼠模型中的突触丧失和认知衰退。
Alzheimers Res Ther. 2025 Jul 21;17(1):168. doi: 10.1186/s13195-025-01813-8.