ArticleMolecular psychiatry2024
Transcriptomic dysregulation and autistic-like behaviors in Kmt2c haploinsufficient mice rescued by an LSD1 inhibitor.
Article in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Do Genetic Variants Directly Shape Population-Level Schizophrenia Burden? A Global Genomic Analysis.Biological psychiatry global open science · 2026Article
- Article
- Autism spectrum disorder risk genes have convergent effects on transcription and neuronal firing patterns in primary neurons.Genome research · 2025Article
- Recapitulation and reversal of neuropsychiatric phenotypes in a mouse model of human endogenous retrovirus type W expression.Molecular psychiatry · 2025Article
- Understanding epigenetic regulation in the endometrium - lessons from mouse models with implantation defects.Epigenomics · 2025Review
- Single-cell technology grows up: Leveraging high-resolution omics approaches to understand neurodevelopmental disorders.Current opinion in neurobiology · 2025Review
- Vafidemstat: a lysine-specific demethylase 1A inhibitor that shows promise for treating neuropsychiatric disorders.Epigenetics reports · 2025Article
Corrections and comments
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Authors and funding
19 authors at 7 institutions in 2 countries.
Funding
Abstract
Recent studies have consistently demonstrated that the regulation of chromatin and gene transcription plays a pivotal role in the pathogenesis of neurodevelopmental disorders. Among many genes involved in these pathways, KMT2C, encoding one of the six known histone H3 lysine 4 (H3K4) methyltransferases in humans and rodents, was identified as a gene whose heterozygous loss-of-function variants are causally associated with autism spectrum disorder (ASD) and the Kleefstra syndrome phenotypic spectrum. However, little is known about how KMT2C haploinsufficiency causes neurodevelopmental deficits and how these conditions can be treated. To address this, we developed and analyzed genetically engineered mice with a heterozygous frameshift mutation of Kmt2c (Kmt2c
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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 Socratic graph.