ReviewCells2022
SAPAP Scaffold Proteins: From Synaptic Function to Neuropsychiatric Disorders.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Pooled it
- Proteomic Characterization of Striatal Neurabin Interactome and Its Sex Specific Impact on Motor Behavior.ACS chemical neuroscience · 2026Article
- The protein interactome of the Neuron Specific Gene family (NSG1-3).bioRxiv : the preprint server for biology · 2025Article
- Proteomic Characterization of Striatal Neurabin Interactome and its Sex Specific Impact on Motor Behavior.bioRxiv : the preprint server for biology · 2025Article
- Allosteric modulation of Grb2 drives ligand-dependent signal responses.Biology direct · 2025Article
- Premorbid characteristics of the SAPAP3 mouse model of obsessive-compulsive disorder: behavior, neuroplasticity, and psilocybin treatment.The international journal of neuropsychopharmacology · 2025Article
- Synaptic editing of frontostriatal circuitry prevents excessive grooming in SAPAP3-deficient mice.bioRxiv : the preprint server for biology · 2025Article
- Resilience mechanisms underlying Alzheimer's disease.Metabolic brain disease · 2025Review
- Late development of OCD-like phenotypes in Dlgap1 knockout mice.Psychopharmacology · 2025Article
- Excitatory/Inhibitory balance in autism spectrum disorders: Integrating genetic, neurotransmitter and computational perspectives.AIMS neuroscience · 2025Review
- Molecular Modeling and In Vitro Functional Analysis of the RGS12 PDZ Domain Variant Associated with High-Penetrance Familial Bipolar Disorder.International journal of molecular sciences · 2024Article
- The effects of different types of social interactions on the electrophysiology of neurons in the nucleus accumbens in rodents.Neuroscience and biobehavioral reviews · 2024Review
- Mapping proteomic composition of excitatory postsynaptic sites in the cerebellar cortex.Frontiers in molecular neuroscience · 2024Article
- The Neurobiological Underpinnings of Obsessive-Compulsive Symptoms in Psychosis, Translational Issues for Treatment-Resistant Schizophrenia.Biomolecules · 2023Review
- Synapse Dysfunctions in Multiple Sclerosis.International journal of molecular sciences · 2023Review
- S-SCAM is essential for synapse formation.Frontiers in cellular neuroscience · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Excitatory (glutamatergic) synaptic transmission underlies many aspects of brain activity and the genesis of normal human behavior. The postsynaptic scaffolding proteins SAP90/PSD-95-associated proteins (SAPAPs), which are abundant components of the postsynaptic density (PSD) at excitatory synapses, play critical roles in synaptic structure, formation, development, plasticity, and signaling. The convergence of human genetic data with recent in vitro and in vivo animal model data indicates that mutations in the genes encoding SAPAP1-4 are associated with neurological and psychiatric disorders, and that dysfunction of SAPAP scaffolding proteins may contribute to the pathogenesis of various neuropsychiatric disorders, such as schizophrenia, autism spectrum disorders, obsessive compulsive disorders, Alzheimer's disease, and bipolar disorder. Here, we review recent major genetic, epigenetic, molecular, behavioral, electrophysiological, and circuitry studies that have advanced our knowledge by clarifying the roles of SAPAP proteins at the synapses, providing new insights into the mechanistic links to neurodevelopmental and neuropsychiatric disorders.
Indexed as
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What Socratic holds
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.