ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Trip6 promotes dendritic morphogenesis through dephosphorylated GRIP1-dependent myosin VI and F-actin organization.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Pubertal development in healthy children is mirrored by DNA methylation patterns in peripheral blood.Scientific reports · 2016Trial
- TRIP6 functions in brain ciliogenesis.Nature communications · 2021Article
- Levels of endocrine-disrupting chemicals are associated with changes in the peri-pubertal epigenome.Endocrine connections · 2020Article
- Article
- Spatial control of membrane traffic in neuronal dendrites.Molecular and cellular neurosciences · 2020Review
- AMPA receptors and their minions: auxiliary proteins in AMPA receptor trafficking.Cellular and molecular life sciences : CMLS · 2019Review
- Expression of Unconventional Myosin VI in Oligodendrocytes.Neurochemical research · 2017Article
- MicroRNA‑138‑5p regulates neural stem cell proliferation and differentiation in vitro by targeting TRIP6 expression.Molecular medicine reports · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
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Abstract
Thyroid receptor-interacting protein 6 (Trip6), a multifunctional protein belonging to the zyxin family of LIM proteins, is involved in various physiological and pathological processes, including cell migration and tumorigenesis. However, the role of Trip6 in neurons remains unknown. Here, we show that Trip6 is expressed in mouse hippocampal neurons and promotes dendritic morphogenesis. Through interaction with the glutamate receptor-interacting protein 1 (GRIP1) and myosin VI, Trip6 is crucial for the total dendritic length and the number of primary dendrites in cultured hippocampal neurons. Trip6 depletion reduces F-actin content and impairs dendritic morphology, and this phenocopies GRIP1 or myosin VI knockdown. Furthermore, phosphorylation of GRIP1(956T) by AKT1 inhibits the interaction between GRIP1 and myosin VI, but facilitates GRIP1 binding to 14-3-3 protein, which is required for regulating F-actin organization and dendritic morphogenesis. Thus, the Trip6-GRIP1-myosin VI interaction and its regulation on F-actin network play a significant role in dendritic morphogenesis.
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Registered trials
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