ArticleNature2017
Kctd13 deletion reduces synaptic transmission via increased RhoA.
Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
98 citing papers in PubMed, 179 citations in OpenAlex.
- Role of olfactory receptor Olfr544 in neuronal cells: Insights into neurite outgrowth and CREB signaling.iScience · 2026Article
- A Global Analysis of the Complex Structural Organization of KCTD Proteins and Their Functional Implications.International journal of molecular sciences · 2026Review
- Review
- How copy number variations shape brain developmental disorders: Unraveling the synaptic puzzle.Psychiatry and clinical neurosciences · 2026Review
- Article
- KCTD Family: Emerging Regulators of GPCR Biased Signaling.Handbook of experimental pharmacology · 2026Review
- Coro1A and TRIM67 collaborate in netrin-dependent neuronal morphogenesis.The Journal of cell biology · 2025Article
- Deciphering copy number variations and gene implications in an Egyptian cohort with autism spectrum disorders.BMC medical genomics · 2025Article
- doc2a and doc2b contribute to locomotor and social behaviors by down-regulating npas4b in zebrafish.BMC biology · 2025Article
- Neurological Insights into 16p11.2- And 22q11.2-Related Disorders: A Mini-Review.Current genomics · 2025Review
- Identification of novel candidate loci for Alzheimer's disease and related dementias by leveraging the shared genetic basis with hippocampal volume.Aging brain · 2025Article
- The Cul3 ubiquitin ligase engages Insomniac as an adaptor to impact sleep and synaptic homeostasis.PLoS genetics · 2025Article
- The pleiotropic spectrum of proximal 16p11.2 CNVs.American journal of human genetics · 2024Review
- Autism Spectrum Disorder Pathogenesis-A Cross-Sectional Literature Review Emphasizing Molecular Aspects.International journal of molecular sciences · 2024Review
- Ubiquitin system mutations in neurological diseases.Trends in biochemical sciences · 2024Review
- Article
- Characterization of alternative splicing during mammalian brain development reveals the extent of isoform diversity and potential effects on protein structural changes.Biology open · 2024Article
- KCTD10 regulates brain development by destabilizing brain disorder-associated protein KCTD13.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A Comprehensive Analysis of the Structural Recognition between KCTD Proteins and Cullin 3.International journal of molecular sciences · 2024Article
- Novel evidence of CNV deletion inFrontiers in pediatrics · 2024Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Copy-number variants of chromosome 16 region 16p11.2 are linked to neuropsychiatric disorders and are among the most prevalent in autism spectrum disorders. Of many 16p11.2 genes, Kctd13 has been implicated as a major driver of neurodevelopmental phenotypes. The function of KCTD13 in the mammalian brain, however, remains unknown. Here we delete the Kctd13 gene in mice and demonstrate reduced synaptic transmission. Reduced synaptic transmission correlates with increased levels of Ras homolog gene family, member A (RhoA), a KCTD13/CUL3 ubiquitin ligase substrate, and is reversed by RhoA inhibition, suggesting increased RhoA as an important mechanism. In contrast to a previous knockdown study, deletion of Kctd13 or kctd13 does not increase brain size or neurogenesis in mice or zebrafish, respectively. These findings implicate Kctd13 in the regulation of neuronal function relevant to neuropsychiatric disorders and clarify the role of Kctd13 in neurogenesis and brain size. Our data also reveal a potential role for RhoA as a therapeutic target in disorders associated with KCTD13 deletion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.