ArticleScience advances2020
Trappc9 deficiency in mice impairs learning and memory by causing imbalance of dopamine D1 and D2 neurons.
Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- A Penetrable AAV2 Capsid Variant for Efficient Intravitreal Gene Delivery to the Retina.Investigative ophthalmology & visual science · 2025Article
- TBC1D15 Inhibits Autophagy of Microglia through Maintaining the Damaged Swelling Lysosome in Alzheimer's Disease.Aging and disease · 2024Article
- Expanding the genetic and phenotypic spectrum of TRAPPC9 and MID2-related neurodevelopmental disabilities: report of two novel mutations, 3D-modelling, and molecular docking studies.Journal of human genetics · 2024Article
- Chronic pharmacologic manipulation of dopamine transmission ameliorates metabolic disturbance in Trappc9-linked brain developmental syndrome.JCI insight · 2024Article
- Genetic Testing for Global Developmental Delay in Early Childhood.JAMA network open · 2024Article
- Nacc1 Mutation in Mice Models Rare Neurodevelopmental Disorder with Underlying Synaptic Dysfunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- A circRNA ceRNA network involved in cognitive dysfunction after chronic cerebral hypoperfusion.Aging · 2024Article
- Case Report: Whole exome sequencing identifies compound heterozygous variants in theFrontiers in genetics · 2024Article
- Circadian rhythm disruptions associated with opioid use disorder in synaptic proteomes of human dorsolateral prefrontal cortex and nucleus accumbens.Molecular psychiatry · 2023Article
- Methionine orchestrates the metabolism vulnerability in cisplatin resistant bladder cancer microenvironment.Cell death & disease · 2023Article
- A novel necroptosis-related long noncoding RNA model for predicting clinical features, immune characteristics, and therapeutic response in clear cell renal cell carcinoma.Frontiers in immunology · 2023Article
- Defective neurite elongation and branching in Nibp/Trappc9 deficient zebrafish and mice.International journal of biological sciences · 2023Article
- Stapled peptide PROTAC induced significantly greater anti-PD-L1 effects than inhibitor in human cervical cancer cells.Frontiers in immunology · 2023Article
- The role of the symbiotic microecosystem in cancer: gut microbiota, metabolome, and host immunome.Frontiers in immunology · 2023Review
- Article
- Impaired XK recycling for importing manganese underlies striatal vulnerability in Huntington's disease.The Journal of cell biology · 2022Article
- Distinct Autism Spectrum Disorder Phenotype and Hand-Flapping Stereotypes: Two Siblings with Novel Homozygous Mutation inMolecular syndromology · 2022Article
- Trappc9 Deficiency Impairs the Plasticity of Stem Cells.International journal of molecular sciences · 2022Article
- Biallelic variants in TRAPPC10 cause a microcephalic TRAPPopathy disorder in humans and mice.PLoS genetics · 2022Article
- Multi-domain computerized cognitive training for children with intellectual developmental disorder: A randomized controlled trial.Frontiers in psychology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic mutations in the gene encoding transport protein particle complex 9 (trappc9), a subunit of TRAPP that acts as a guanine nucleotide exchange factor for rab proteins, cause intellectual disability with brain structural malformations by elusive mechanisms. Here, we report that trappc9-deficient mice exhibit a broad range of behavioral deficits and postnatal delay in growth of the brain. Contrary to volume decline of various brain structures, the striatum of trappc9 null mice was enlarged. An imbalance existed between dopamine D1 and D2 receptor containing neurons in the brain of trappc9-deficient mice; pharmacological manipulation of dopamine receptors improved performances of trappc9 null mice to levels of wild-type mice on cognitive tasks. Loss of trappc9 compromised the activation of rab11 in the brain and resulted in retardation of endocytic receptor recycling in neurons. Our study elicits a pathogenic mechanism and a potential treatment for trappc9-linked disorders including intellectual disability.
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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.