ArticleTranslational psychiatry2024
Gatad2b, associated with the neurodevelopmental syndrome GAND, plays a critical role in neurodevelopment and cortical patterning.
Article in Translational psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Multicomplex Integrative Structural Modeling of a Human Histone Deacetylase Interactome.bioRxiv : the preprint server for biology · 2026Article
- Identification of Immune-Related Lactylation Genes in Rheumatoid Arthritis With Atherosclerosis: A Comprehensive Analysis Using Bulk and Single-Cell RNA Sequencing Data.Mediators of inflammation · 2026Article
- Restoring Retinoic Acid: Alleviating Autism-Like Behaviors in Sox5-Deficient Mice.Neuroscience bulletin · 2025Article
- GATA Transcription Factors: A Cross-Road for Erythropoiesis, Neurodevelopment, and Synucleinopathies.Developmental neurobiology · 2025Review
- GATAD2B-related developmental and epileptic encephalopathy (DEE): Extending the epilepsy phenotype and a literature appraisal.Epilepsia open · 2025Review
- Cortical arealization of interneurons defines shared and distinct molecular programs in developing human and macaque brains.Nature communications · 2025Article
- Prediction and assessment of deleterious and disease causing nonsynonymous single nucleotide polymorphisms (nsSNPs) in humanHeliyon · 2024Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
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Abstract
GATAD2B (GATA zinc finger domain containing 2B) variants are associated with the neurodevelopmental syndrome GAND, characterized by intellectual disability (ID), infantile hypotonia, apraxia of speech, epilepsy, macrocephaly and distinct facial features. GATAD2B encodes for a subunit of the Nucleosome Remodeling and Histone Deacetylase (NuRD) complex. NuRD controls transcriptional programs critical for proper neurodevelopment by coupling histone deacetylase with ATP-dependent chromatin remodeling activity. To study mechanisms of pathogenesis for GAND, we characterized a mouse model harboring an inactivating mutation in Gatad2b. Homozygous Gatad2b mutants die perinatally, while haploinsufficient Gatad2b mice exhibit behavioral abnormalities resembling the clinical features of GAND patients. We also observed abnormal cortical patterning, and cellular proportions and cell-specific alterations in the developmental transcriptome in these mice. scRNAseq of embryonic cortex indicated misexpression of genes key for corticogenesis and associated with neurodevelopmental syndromes such as Bcl11b, Nfia and H3f3b and Sox5. These data suggest a crucial role for Gatad2b in brain development.
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