ReviewPharmacological reviews2016
Kinase-dependent Regulation of Monoamine Neurotransmitter Transporters.
Review in Pharmacological reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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
66 citing papers in PubMed, 99 citations in OpenAlex.
- No Evidence of Moderated Impulsivity Following Administration of the IMPase Inhibitor Ebselen in Healthy Adults.Human psychopharmacology · 2026Trial
- Multicolor Quantum Dot Tracking Uncovers Phenotypic Rescue of DAT A559V Aberrant Diffusion Upon D2R Antagonism.ACS chemical neuroscience · 2026Article
- Recent Advances and Emerging Pharmacotherapeutic Approaches for Central Hypersomnolence Disorders.Clinical pharmacology : advances and applications · 2026Review
- Transient Suppression of Dopamine Transporter Palmitoylation by Methamphetamine: Implications for Transport Regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Multidimensional Evaluation of Lisdexamfetamine: Pharmacology, Therapeutic Use, Toxicity and Forensic Implications.Basic & clinical pharmacology & toxicology · 2025Review
- Kappa opioid receptor antagonism restores phosphorylation, trafficking and behavior induced by a disease-associated dopamine transporter variant.Molecular psychiatry · 2025Article
- A Common Cause of ADHD and Bipolar Disorder (BD).Bipolar disorders · 2025Article
- Threonine-53 Phosphorylation of Dopamine Transporter Dictates κ-Opioid Receptor-Mediated Locomotor Suppression, Aversion, and Cocaine Reward.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Causal Mechanisms of Monoamine Transporter Phosphorylation.Advances in neurobiology · 2025Review
- Pathogenic variants at the N-terminal arginine residue 44 disrupt human GABA transporter 1 function: insights fromFrontiers in pharmacology · 2025Article
- Monoamine signaling and neuroinflammation: mechanistic connections and implications for neuropsychiatric disorders.Frontiers in immunology · 2025Review
- Modulation of serotonin transporter expression by escitalopram under inflammation.Communications biology · 2024Article
- Serotonin and the serotonin transporter in the adrenal gland.Vitamins and hormones · 2024Review
- Functional and pathological consequences of being fast on the uptake: Protein kinase G and p38α MAPK regulation of serotonin transporters.Current research in physiology · 2024Review
- α7 Nicotinic acetylcholine receptor: a key receptor in the cholinergic anti-inflammatory pathway exerting an antidepressant effect.Journal of neuroinflammation · 2023Review
- Presynaptic Gq-coupled receptors drive biphasic dopamine transporter trafficking that modulates dopamine clearance and motor function.The Journal of biological chemistry · 2023Article
- Construction and validation of a risk model based on the key SNARE proteins to predict the prognosis and immune microenvironment of gliomas.Frontiers in molecular neuroscience · 2023Article
- Dopamine transporter membrane mobility is bidirectionally regulated by phosphorylation and palmitoylation.Current research in physiology · 2023Review
- Article
- Article
6 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Modulation of neurotransmission by the monoamines dopamine (DA), norepinephrine (NE), and serotonin (5-HT) is critical for normal nervous system function. Precise temporal and spatial control of this signaling in mediated in large part by the actions of monoamine transporters (DAT, NET, and SERT, respectively). These transporters act to recapture their respective neurotransmitters after release, and disruption of clearance and reuptake has significant effects on physiology and behavior and has been linked to a number of neuropsychiatric disorders. To ensure adequate and dynamic control of these transporters, multiple modes of control have evolved to regulate their activity and trafficking. Central to many of these modes of control are the actions of protein kinases, whose actions can be direct or indirectly mediated by kinase-modulated protein interactions. Here, we summarize the current state of our understanding of how protein kinases regulate monoamine transporters through changes in activity, trafficking, phosphorylation state, and interacting partners. We highlight genetic, biochemical, and pharmacological evidence for kinase-linked control of DAT, NET, and SERT and, where applicable, provide evidence for endogenous activators of these pathways. We hope our discussion can lead to a more nuanced and integrated understanding of how neurotransmitter transporters are controlled and may contribute to disorders that feature perturbed monoamine signaling, with an ultimate goal of developing better therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.