ArticleJournal of molecular neuroscience : MN2021
Expression Analysis of VDR-Related LncRNAs in Autism Spectrum Disorder.
Article in Journal of molecular neuroscience : MN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 11 citations in OpenAlex.
- The Vitamin D-Gut-Brain Axis in Autism Spectrum Disorder: A Bidirectional Crosstalk.International journal of general medicine · 2026Review
- Article
- Sex-Specific effects of vitamin D on autistic behavior and gastrointestinal symptoms in rats via the regulation of serotonin metabolism.Scientific reports · 2025Article
- Human Blood-Derived lncRNAs in Autism Spectrum Disorder.Biomolecules · 2025Review
- Exploring the Missing link between vitamin D and autism spectrum disorder: Scientific evidence and new perspectives.Heliyon · 2024Article
- Tracing vitamins on the long non-coding lane of the transcriptome: vitamin regulation of LncRNAs.Genes & nutrition · 2024Review
- Upregulation of VDR-associated lncRNAs in Schizophrenia.Journal of molecular neuroscience : MN · 2022Article
- Emerging Role of Non-coding RNAs in Autism Spectrum Disorder.Journal of molecular neuroscience : MN · 2022Review
- Expression Analysis of Ermin and Listerin E3 Ubiquitin Protein Ligase 1 Genes in Autistic Patients.Frontiers in molecular neuroscience · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitamin D receptor (VDR) signaling has been reported to affect neurodevelopment, thus participating in the risk of autism spectrum disorder (ASD). We have measured expression amounts of VDR, CYP27B1, and two related long non-coding RNAs, namely SNHG6 and LINC00511, in the circulation of ASD patients compared with normal controls. Expression of CYP27B1 was remarkably higher in ASD cases compared with controls (posterior beta = 2.38, SE = 0.46, adjusted P value < 0.0001, 95% credible interval (CrI) for beta = [1.49, 3.27]). Level of SNHG6 was lower in ASD cases compared with controls (posterior beta = - 0.791, SE = 0.24, adjusted P value = 0.029, 95% CrI for beta = [- 1.27, - 0.33]). Expression levels of VDR and LINC00511 were similar between ASD cases and controls (P values = 0.97 and 0.46, respectively). Expressions of VDR, CYP27B1, SNHG6, and LINC00511 were not correlated with age of children. However, significant correlations were perceived between expressions of CYP27B1 and LINC00511 (r = 0.47, P < 0.0001), VDR and CYP27B1 (r = 0.42, P < 0.0001), and VDR and SNHG6 (r = 0.32, P < 0.0001). Therefore, these results imply dysregulation of a number of VDR-related genes in ASD patients.
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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.