SynthesisAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2020
MYT1L: A systematic review of genetic variation encompassing schizophrenia and autism.
Synthesis in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Genetic risk factors for autism-spectrum disorders: a systematic review based on systematic reviews and meta-analysis.Journal of neural transmission (Vienna, Austria : 1996) · 2021Pooled it
- A Novel Variant in the MYT1L Gene Shared by Three Individuals with Neuropsychiatric and Neurodevelopmental Manifestations in a Family.Indian journal of psychological medicine · 2026Article
- Neurobehavioral Profiles and Clinical Consequences ofmedRxiv : the preprint server for health sciences · 2025Article
- Exploring the bidirectional causal relationship between Autism Spectrum Disorder and Schizophrenia using Mendelian randomization.Medicine · 2025Article
- Autism- and intellectual disability-associated MYT1L mutation alters human cortical interneuron differentiation, maturation, and physiology.Stem cell reports · 2025Article
- Chromosomal and gonadal sex have differing effects on social motivation in mice.Biology of sex differences · 2025Article
- Chromosomal and gonadal sex have differing effects on social motivation in mice.bioRxiv : the preprint server for biology · 2024Article
- Prenatal exposure to common infections and newborn DNA methylation: A prospective, population-based study.Brain, behavior, and immunity · 2024Article
- The Use of CGH Arrays for Identifying Copy Number Variations in Children with Autism Spectrum Disorder.Brain sciences · 2024Article
- 2p25.3 microduplications involving MYT1L: further phenotypic characterization through an assessment of 16 new cases and a literature review.European journal of human genetics : EJHG · 2023Review
- MYT1L haploinsufficiency in human neurons and mice causes autism-associated phenotypes that can be reversed by genetic and pharmacologic intervention.Molecular psychiatry · 2023Article
- BRG1: Promoter or Suppressor of Cancer? The Outcome of BRG1's Interaction with Specific Cellular Pathways.International journal of molecular sciences · 2023Review
- Exposure to war and conflict: The individual and inherited epigenetic effects on health, with a focus on post-traumatic stress disorder.Frontiers in epidemiology · 2023Review
- Systematic analysis of copy number variants of uncertain significance partially overlapping with the haploinsufficient or triplosensitive genes in clinical testing.Annals of medicine · 2023Article
- Regulation of human cortical interneuron development by the chromatin remodeling protein CHD2.Scientific reports · 2022Article
- MYT1L in the making: emerging insights on functions of a neurodevelopmental disorder gene.Translational psychiatry · 2022Review
- Myt1l haploinsufficiency leads to obesity and multifaceted behavioral alterations in mice.Molecular autism · 2022Article
- Article
- MYT1L-associated neurodevelopmental disorder: description of 40 new cases and literature review of clinical and molecular aspects.Human genetics · 2022Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Variations in MYT1L, a gene encoding a transcription factor expressed in the brain, have been associated with autism, intellectual disability, and schizophrenia. Here we provide an updated review of published reports of neuropsychiatric correlates of loss of function and duplication of MYT1L. Of 27 duplications all were partial; 33% were associated exclusively with schizophrenia, and the chromosomal locations of schizophrenia-associated duplications exhibited a distinct difference in pattern-of-location from those associated with autism and/or intellectual disability. Of 51 published heterozygous loss of function variants, all but one were associated with intellectual disability, autism, or both, and one resulted in no neuropsychiatric diagnosis. There were no reports of schizophrenia associated with loss of function variants of MYT1L (Fisher's exact p < .00001, for contrast with all reported duplications). Although the precise function of the various mutations remains unspecified, these data collectively establish the candidacy of MYT1L as a reciprocal mutation, in which schizophrenia may be engendered by partial duplications, typically involving the 3' end of the gene, while developmental disability-notably autism-is associated with both loss of function and partial duplication. Future research on the specific effects of contrasting mutations in MYT1L may provide insight into the causal origins of autism and schizophrenia.
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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.