ArticleNeuroscience letters2016
Tsc1 haploinsufficiency is sufficient to increase dendritic patterning and Filamin A levels.
Article in Neuroscience letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Beyond mTOR: Unraveling the Complex Pathophysiology and Signaling Pathways in Focal Cortical Dysplasia.Molecular neurobiology · 2025Review
- Filamin A in focus: unravelling the multifaceted roles of filamin A in neurodevelopment and neurological disorders.Brain : a journal of neurology · 2025Review
- Reducing Filamin A Restores Cortical Synaptic Connectivity and Early Social Communication Following Cellular Mosaicism in Autism Spectrum Disorder Pathways.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Primary cells derived from Tuberous Sclerosis Complex patients show autophagy alteration in the haploinsufficiency state.Genetics and molecular biology · 2021Article
- Convergent and Divergent Mechanisms of Epileptogenesis in mTORopathies.Frontiers in neuroanatomy · 2021Review
- Filamin A inhibition reduces seizure activity in a mouse model of focal cortical malformations.Science translational medicine · 2020Article
- Role of mTOR Complexes in Neurogenesis.International journal of molecular sciences · 2018Review
- Fil-lamin-ing in the Gap in Cortical Dysplasia.Epilepsy currentsArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Most individuals with tuberous sclerosis complex (TSC) are born with a mutant allele of either TSC1 or TSC2 and a mosaic of psychological and cognitive defects. Tsc1 loss of heterozygosity contributes to severe dendritic abnormalities that are rescued by normalizing the levels of the actin-cross linking protein, Filamin A (FLNA). However, it is unclear whether dendrites and FLNA levels are abnormal in an heterozygote Tsc1 condition. Here, we examined dendritic morphology and FLNA levels in the olfactory bulb of Tsc1 wild type and heterozygote mice. Using in vivo neonatal electroporation to label newborn neurons followed by sholl analysis, we found that Tsc1 haploinsufficiency is associated with increased dendritic complexity and total dendritic length as well as increased FLNA levels. Since reducing FLNA levels has been shown to decrease Tsc1(+/-) dendritic complexity, these data suggest that increased FLNA levels in Tsc1(+/-) mice contribute to abnormal dendritic patterning in the Tsc1 heterozygote condition of individuals with TSC.
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Registered trials
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