ReviewTranslational psychiatry2022
MYT1L in the making: emerging insights on functions of a neurodevelopmental disorder gene.
Review in Translational psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Temporal Transcriptional Regulation of Human Neuronal Differentiation via Forward Programming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neurobehavioral Profiles and Clinical Consequences ofmedRxiv : the preprint server for health sciences · 2025Article
- Paracrine Bone-Derived Senescent Secretome Induces Spatially Patterned ECM and Biomechanical Vulnerability in Human Brain Organoids.bioRxiv : the preprint server for biology · 2025Article
- A survey of hypothalamic phenotypes identifies molecular and behavioral consequences of MYT1L haploinsufficiency in male and female mice.Hormones and behavior · 2025Article
- Direct reprogramming of fibroblasts into spiral ganglion neurons by defined transcription factors.Cell proliferation · 2025Article
- Stimulus-Dependent Expression ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Coordinated neuron-specific splicing events restrict nucleosome engagement of the LSD1 histone demethylase complex.Cell reports · 2025Article
- Cross-species analyses of thymic mimetic cells reveal evolutionarily ancient origins and both conserved and species-specific elements.Immunity · 2025Article
- MYT1L deficiency impairs excitatory neuron trajectory during cortical development.Nature communications · 2024Article
- Genomic insights into genes expressed specifically during infancy highlight their dominant influence on the neuronal system.BMC genomics · 2024Article
- Prenatal exposure to common infections and newborn DNA methylation: A prospective, population-based study.Brain, behavior, and immunity · 2024Article
- A multiomic atlas of the aging hippocampus reveals molecular changes in response to environmental enrichment.Nature communications · 2024Article
- A Comprehensive Review of Syndromic Forms of Obesity: Genetic Etiology, Clinical Features and Molecular Diagnosis.Current obesity reports · 2024Review
- Asynchronous microexon splicing ofbioRxiv : the preprint server for biology · 2024Article
- Risk factors and related miRNA phenotypes of chronic pain after thoracoscopic surgery in lung adenocarcinoma patients.PloS one · 2024Article
- Article
- Multi-omics approach reveals dysregulated genes during hESCs neuronal differentiation exposure to paracetamol.iScience · 2023Article
- MYT1L is required for suppressing earlier neuronal development programs in the adult mouse brain.Genome research · 2023Article
- Differential Expression of microRNAs in Serum of Patients with Chronic Painful Polyneuropathy and Healthy Age-Matched Controls.Biomedicines · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Large scale human genetic studies have shown that loss of function (LoF) mutations in MYT1L are implicated in neurodevelopmental disorders (NDDs). Here, we provide an overview of the growing number of published MYT1L patient cases, and summarize prior studies in cells, zebrafish, and mice, both to understand MYT1L's molecular and cellular role during brain development and consider how its dysfunction can lead to NDDs. We integrate the conclusions from these studies and highlight conflicting findings to reassess the current model of the role of MYT1L as a transcriptional activator and/or repressor based on the biological context. Finally, we highlight additional functional studies that are needed to understand the molecular mechanisms underlying pathophysiology and propose key questions to guide future preclinical studies.
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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.