ArticleMolecular autism2022
Autism-associated protein POGZ controls ESCs and ESC neural induction by association with esBAF.
Article in Molecular autism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- CRISPR-engineered deletion of POGZ alters transcription factor binding at promoters of genes involved in synaptic signaling.HGG advances · 2026Article
- Reciprocal regulation between autism risk gene POGZ and circadian clock.JCI insight · 2026Article
- The Zinc-Finger Protein POGZ Associates with Polycomb Repressive Complex 1 to Regulate Bone Morphogenetic Protein Signaling During Neuronal Differentiation.Stem cell reviews and reports · 2026Article
- Mix-and-match between transposable elements and zinc finger proteins fuels genic and regulatory innovation.Current opinion in genetics & development · 2025Review
- CRISPR-engineered deletion ofbioRxiv : the preprint server for biology · 2025Article
- Retrotransposon: an insight into neurological disorders from perspectives of neurodevelopment and aging.Translational neurodegeneration · 2025Review
- A novel nonsense variant inHeliyon · 2024Article
- O-GlcNAc transferase congenital disorder of glycosylation (OGT-CDG): Potential mechanistic targets revealed by evaluating the OGT interactome.The Journal of biological chemistry · 2024Review
- Genetic and Environmental Factors Co-Contributing to Behavioral Abnormalities inInternational journal of molecular sciences · 2024Article
- Molecular landscape of congenital vertebral malformations: recent discoveries and future directions.Orphanet journal of rare diseases · 2024Review
- Epigenetic regulation of craniofacial development and disease.Birth defects research · 2024Review
- Deficiency ofBrain communications · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe POGZ gene has been found frequently mutated in neurodevelopmental disorders (NDDs), particularly autism spectrum disorder (ASD) and intellectual disability (ID). However, little is known about its roles in embryonic stem cells (ESCs), neural development and diseases.
methodsWe generated Pogz-/- ESCs and directed ESC differentiation toward a neural fate. We performed biochemistry, ChIP-seq, ATAC-seq, and bioinformatics analyses to understand the role of POGZ.
resultsWe show that POGZ is required for the maintenance of ESC identity and the up-regulation of neural genes during ESC differentiation toward a neural fate. Genome-wide binding analysis shows that POGZ is primarily localized to gene promoter and enhancer regions. POGZ functions as both a transcriptional activator and repressor, and its loss leads to deregulation of differentiation genes, including neural genes. POGZ physically associates with the SWI-SNF (esBAF) chromatin remodeler complex, and together they modulate enhancer activities via epigenetic modifications such as chromatin remodeling and histone modification. During ESC neural induction, POGZ-mediated recruitment of esBAF/BRG1 and H3K27ac are important for proper expression of neural progenitor genes. LIMITATIONS: The genotype and allele relevant to human neurodevelopmental disorders is heterozygous loss of function. This work is designed to study the effects of loss of POGZ function on ESCs and during ESC neural induction. Also, this work lacks of in vivo validation using animal models.
conclusionsThe data suggest that POGZ is both a transcription factor and a genome regulator, and its loss leads to defects in neural induction and neurogenesis.
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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.