TRPC4 deletion elicits behavioral defects in sociability by dysregulating expression of microRNA-138-2.

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作者： Jee Young,Seo ^[1] ; Hye-Ryeong,Jo ^[2] ; Seung Hoon,Lee ^[2] ; Do Gyeong,Kim ^[1] ; Huiju,Lee ^[1] ; Ye Lim,Kim ^[1] ; Young In,Choi ^[3] ; Sung Jun,Jung ^[1] ; Hyeon,Son ^[3]

作者单位： Graduate School of Biomedical Science and Engineering, Hanyang Biomedical Research Institute, Hanyang University, 222 Wangsimni-ro, Seongdong-gu, Seoul, Korea. ^[1] Hanyang University Hospital for Rheumatic Diseases, 222 Wangsimni-ro, Seongdong-gu, Seoul, Korea. ^[2] Department of Physiology, College of Medicine, Hanyang University, 222 Wangsimni-ro, Seongdong-gu, Seoul, Korea. ^[3] Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, 222 Wangsimni-ro, Seongdong-gu, Seoul, Korea. ^[4]

关键词 Behavioral neuroscience Molecular neuroscience Neuroscience Rodent behavior

DOI 10.1016/j.isci.2023.108617

PMID 38188509

发布时间 2024-01-09

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2024年27卷1期

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TRPC4 deletion elicits behavioral defects in sociability by dysregulating expression of microRNA-138-2.

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TRPC4 deletion elicits behavioral defects in sociability by dysregulating expression of microRNA-138-2.

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