ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Targeting of acetylcholinesterase in neurons in vivo: a dual processing function for the proline-rich membrane anchor subunit and the attachment domain on the catalytic subunit.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 65 citations in OpenAlex.
- The Novel Functions of M4 Muscarinic Receptors.Physiological research · 2025Review
- Molecular Analysis of a Congenital Myasthenic Syndrome Due to a Pathogenic Variant Affecting the C-Terminus of ColQ.International journal of molecular sciences · 2023Article
- Striatal Cholinergic Signaling in Time and Space.Molecules (Basel, Switzerland) · 2022Review
- Cholinesterases in Tripartite Neuromuscular Synapse.Frontiers in molecular neuroscience · 2021Review
- Characterization of Human Genes Modulated byFrontiers in immunology · 2021Article
- Forebrain Cholinergic Signaling: Wired and Phasic, Not Tonic, and Causing Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Review
- Targeted sequencing of linkage region in Dominican families implicates PRIMA1 and the SPATA7-PTPN21-ZC3H14-EML5-TTC8 locus in carotid-intima media thickness and atherosclerotic events.Scientific reports · 2019Article
- Optogenetic augmentation of the hypercholinergic endophenotype in DYT1 knock-in mice induced erratic hyperactive movements but not dystonia.EBioMedicine · 2019Article
- Colorectal adenoma and cancer detection based on altered methylation pattern of SFRP1, SFRP2, SDC2, and PRIMA1 in plasma samples.Epigenetics · 2017Article
- In Vitro Innervation as an Experimental Model to Study the Expression and Functions of Acetylcholinesterase and Agrin in Human Skeletal Muscle.Molecules (Basel, Switzerland) · 2017Review
- Ultrafast and Slow Cholinergic Transmission. Different Involvement of Acetylcholinesterase Molecular Forms.Molecules (Basel, Switzerland) · 2017Review
- Increased Expression of Readthrough Acetylcholinesterase Variants in the Brains of Alzheimer's Disease Patients.Journal of Alzheimer's disease : JAD · 2016Article
- What do phasic cholinergic signals do?Neurobiology of learning and memory · 2016Review
- Aberrant DNA Methylation of rDNA and PRIMA1 in Borderline Personality Disorder.International journal of molecular sciences · 2016Article
- PRIMA1 mutation: a new cause of nocturnal frontal lobe epilepsy.Annals of clinical and translational neurology · 2015Article
- Dysfunctional Presynaptic M2 Receptors in the Presence of Chronically High Acetylcholine Levels: Data from the PRiMA Knockout Mouse.PloS one · 2015Article
- Schwann cells sense and control acetylcholine spillover at the neuromuscular junction by α7 nicotinic receptors and butyrylcholinesterase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Reassessment of the role of the central cholinergic system.Journal of molecular neuroscience : MN · 2014Review
- Proteomic screening of glutamatergic mouse brain synaptosomes isolated by fluorescence activated sorting.The EMBO journal · 2014Article
- Neuronal AChE splice variants and their non-hydrolytic functions: redefining a target of AChE inhibitors?British journal of pharmacology · 2013Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Acetylcholinesterase (AChE) accumulates on axonal varicosities and is primarily found as tetramers associated with a proline-rich membrane anchor (PRiMA). PRiMA is a small transmembrane protein that efficiently transforms secreted AChE to an enzyme anchored on the outer cell surface. Surprisingly, in the striatum of the PRiMA knock-out mouse, despite a normal level of AChE mRNA, we find only 2-3% of wild type AChE activity, with the residual AChE localized in the endoplasmic reticulum, demonstrating that PRiMA in vivo is necessary for intracellular processing of AChE in neurons. Moreover, deletion of the retention signal of the AChE catalytic subunit in mice, which is the domain of interaction with PRiMA, does not restore AChE activity in the striatum, establishing that PRiMA is necessary to target and/or to stabilize nascent AChE in neurons. These unexpected findings open new avenues to modulating AChE activity and its distribution in CNS disorders.
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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.