ArticleCell death & disease2018
MARVELD1 depletion leads to dysfunction of motor and cognition via regulating glia-dependent neuronal migration during brain development.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
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- The regulation loop of MARVELD1 interacting with PARP1 in DNA damage response maintains genome stability and promotes therapy resistance of cancer cells.Cell death and differentiation · 2023Article
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- Delayed cortical development in mice with a neural specific deletion of β1 integrin.Frontiers in neuroscience · 2023Article
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- Animal models of the placenta accreta spectrum: current status and further perspectives.Frontiers in endocrinology · 2023Review
- KIF5C deficiency causes abnormal cortical neuronal migration, dendritic branching, and spine morphology in mice.Pediatric research · 2022Article
- Paeoniflorin Alleviates Skeletal Muscle Atrophy in Ovariectomized Mice through the ERα/NRF1 Mitochondrial Biogenesis Pathway.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Article
- Up-regulation of MARVEL domain-containing protein 1 (MARVELD1) accelerated the malignant phenotype of glioma cancer cells via mediating JAK/STAT signaling pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The establishment of functional neuronal connectivity is dependent on the neuronal migration and the accurate positioning of neurons in the developing brain. Abnormal neuronal migration can trigger neuronal maturation defects and apoptosis. However, many genetic bases remain unclear in neuronal migration disorders during brain development. In this study, we reported that MARVELD1-defected mice displayed motor and cognitive dysfunction resulting from aberrant neuronal migration during brain development. The laminar organization of the cerebral cortex and cerebellum in MARVELD1 knockout (KO) mice is disrupted, indicating impaired radial neuronal migration. Furthermore, we used the cerebellum as a model to explore the radial neuronal migration processes, and the results demonstrated that the proper neuronal migration depended on MARVELD1 expression in glial cells of the developing brain. MARVELD1 suppressed the expression of ITGB1 and FAK Tyr397 phosphorylation in glia-dependent manner. The inhibition of the MARVELD1/ITGB1/FAK signalling pathway in MARVELD1 KO mice could reverse the defects in neuronal migration in vitro. Our findings revealed that MARVELD1 regulated neuronal migration by mediating the formation of glial fibres and ITGB1/FAK signalling pathway. The depletion of MARVELD1 during mouse brain development led to the abnormity of motor and cognition functions.
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