ArticlePloS one2014
The DCR protein TTC3 affects differentiation and Golgi compactness in neurons through specific actin-regulating pathways.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 39 citations in OpenAlex.
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- A sensitive and specific non-invasive urine biomarker panel for prostate cancer detection.EBioMedicine · 2025Article
- The lncRNA Snhg11, a new candidate contributing to neurogenesis, plasticity, and memory deficits in Down syndrome.Molecular psychiatry · 2024Article
- Transcriptional consequences of trisomy 21 on neural induction.Frontiers in cellular neuroscience · 2024Article
- An Alzheimer's disease risk variant in TTC3 modifies the actin cytoskeleton organization and the PI3K-Akt signaling pathway in iPSC-derived forebrain neurons.Neurobiology of aging · 2023Article
- The lncRNA Snhg11, a new candidate contributing to neurogenesis, plasticity and memory deficits in Down syndrome.Research square · 2023Article
- Dysregulation of ribosome-associated quality control elicits cognitive disorders via overaccumulation of TTC3.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- TTC3-Mediated Protein Quality Control, A Potential Mechanism for Cognitive Impairment.Cellular and molecular neurobiology · 2022Review
- Of rings and spines: The multiple facets of Citron proteins in neural development.Small GTPases · 2020Review
- TTC3 contributes to TGF-βCell death & disease · 2019Article
- Embryonic atrazine exposure elicits proteomic, behavioral, and brain abnormalities with developmental time specific gene expression signatures.Journal of proteomics · 2018Article
- An Integrated Human/Murine Transcriptome and Pathway Approach To Identify Prenatal Treatments For Down Syndrome.Scientific reports · 2016Article
- DYRK1A haploinsufficiency causes a new recognizable syndrome with microcephaly, intellectual disability, speech impairment, and distinct facies.European journal of human genetics : EJHG · 2015Article
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
In neuronal cells, actin remodeling plays a well known role in neurite extension but is also deeply involved in the organization of intracellular structures, such as the Golgi apparatus. However, it is still not very clear which mechanisms may regulate actin dynamics at the different sites. In this report we show that high levels of the TTC3 protein, encoded by one of the genes of the Down Syndrome Critical Region (DCR), prevent neurite extension and disrupt Golgi compactness in differentiating primary neurons. These effects largely depend on the capability of TTC3 to promote actin polymerization through signaling pathways involving RhoA, ROCK, CIT-N and PIIa. However, the functional relationships between these molecules differ significantly if considering the TTC3 activity on neurite extension or on Golgi organization. Finally, our results reveal an unexpected stage-dependent requirement for F-actin in Golgi organization at different stages of neuronal differentiation.
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