ArticleNature neuroscience2008
Palmitoylation-dependent neurodevelopmental deficits in a mouse model of 22q11 microdeletion.
Article in Nature neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 2 of them syntheses 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
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Who cites it
156 citing papers in PubMed, 2 syntheses or guidelines pooled it, 266 citations in OpenAlex.
- Magnitude and heterogeneity of brain structural abnormalities in 22q11.2 deletion syndrome: a meta-analysis.Molecular psychiatry · 2020Pooled it
- Dissociation of Golgi-associated DHHC-type Zinc Finger Protein (GODZ)- and Sertoli Cell Gene with a Zinc Finger Domain-β (SERZ-β)-mediated Palmitoylation by Loss of Function Analyses in Knock-out Mice.The Journal of biological chemistry · 2016Guideline
- 5q31 duplications encompassing PURA are associated with a neurodevelopmental disorder.European journal of human genetics : EJHG · 2026Article
- Article
- ZDHHC8-mediated S-palmitoylation of RAD21 causes mitochondrial dysfunction in diabetic nephropathy via inhibiting ACSM3 transcription.Cell death and differentiation · 2026Article
- Gene dosage effects of 22q11.2 copy number variants on in-vivo measures of white matter axonal density and dispersion.Molecular psychiatry · 2026Article
- Unraveling the enigma: Post-translational modifications in psychiatric disorders and their regulatory mechanisms.Journal of translational internal medicine · 2026Article
- The Causal Relationship Between Palmitoylation Genes and Parkinson's Disease: A Mendelian Randomization Study.Journal of molecular neuroscience : MN · 2025Article
- Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome-associated schizophrenia.Nature communications · 2025Article
- Fat traffic control: S-acylation in axonal transport.Molecular pharmacology · 2025Review
- Article
- Fine Regulation of MicroRNAs in Gene Regulatory Networks and Pathophysiology.International journal of molecular sciences · 2025Review
- Synaptic-dependent developmental dysconnectivity in 22q11.2 deletion syndrome.Science advances · 2025Article
- Review
- Article
- Altered Protein Palmitoylation as Disease Mechanism in Neurodegenerative Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Review
- Palmitoylation of synaptic proteins: roles in functional regulation and pathogenesis of neurodegenerative diseases.Cellular & molecular biology letters · 2024Review
- Mechanisms and functions of protein S-acylation.Nature reviews. Molecular cell biology · 2024Review
- Synaptic-dependent developmental dysconnectivity in 22q11.2 deletion syndrome.bioRxiv : the preprint server for biology · 2024Article
- DiGeorge syndrome critical region gene 2 (DGCR2), a schizophrenia risk gene, regulates dendritic spine development through cell adhesion.Cell & bioscience · 2023Article
96 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Individuals with 22q11.2 microdeletions have cognitive deficits and a high risk of developing schizophrenia. Here we provide evidence that primary hippocampal neurons from a mouse model of 22q11.2 deletion (Df(16)A(+/-) mice) have decreased density of dendritic spines and glutamatergic synapses, as well as impaired dendritic growth. These deficits were prevented by introduction of the enzymatically active ZDHHC8 palmitoyltransferase encoded by a gene in the 22q11.2 locus, and they were also observed in primary cultures from Zdhhc8-deficient mice. Many of these deficits were also present in the hippocampi of adult Df(16)A(+/-) and Zdhhc8-deficient mice. Finally, we provide evidence that PSD95 is one of the substrates of ZDHHC8. Our analysis reveals that 22q11.2 microdeletion results in deficits in neuronal development and suggests that impaired neuronal protein palmitoylation contributes to many of these deficits.
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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.