ReviewNeuromolecular medicine2005
Once and future signaling: G protein-coupled receptor kinase control of neuronal sensitivity.
Review in Neuromolecular medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 25 citations in OpenAlex.
- Sex differences in stress-related psychiatric disorders: neurobiological perspectives.Frontiers in neuroendocrinology · 2014Review
- Sex differences in molecular and cellular substrates of stress.Cellular and molecular neurobiology · 2012Review
- S-nitrosylation-regulated GPCR signaling.Biochimica et biophysica acta · 2012Article
- Molecular and cellular sex differences at the intersection of stress and arousal.Neuropharmacology · 2012Review
- Differential effects of inescapable stress on locus coeruleus GRK3, alpha2-adrenoceptor and CRF1 receptor levels in learned helpless and non-helpless rats: a potential link to stress resilience.Behavioural brain research · 2011Article
- Discontinuous pH gradient-mediated separation of TiO2-enriched phosphopeptides.Analytical biochemistry · 2011Article
- Role of Beta-arrestin 2 downstream of dopamine receptors in the Basal Ganglia.Frontiers in neuroanatomy · 2011Article
- Sex differences in corticotropin-releasing factor receptor signaling and trafficking: potential role in female vulnerability to stress-related psychopathology.Molecular psychiatry · 2010Article
- Regulation of serotonin 1B receptor by glycogen synthase kinase-3.Molecular pharmacology · 2009Article
- Chronic adrenaline treatment fails to down-regulate the Del301-303-alpha2B-adrenoceptor in neuronal cells.British journal of pharmacology · 2009Article
- Adaptor protein-2 interaction with arrestin regulates GPCR recycling and apoptosis.Traffic (Copenhagen, Denmark) · 2009Article
- Promoter variant in the GRK3 gene associated with bipolar disorder alters gene expression.Biological psychiatry · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G protein-coupled receptors (GPCRs) are the most numerous class of cell surface receptor, and substances acting through GPCRs mediate many critical signaling events and physiological processes. GPCR sensitivity and signaling is dynamic, responding rapidly to adjust to changes in the ambient level of stimulation of target cells. One important mediator of such receptor sensitivity is the family of GPCR kinases (GRKs). Like heterotrimeric G proteins, GRKs recognize agonist-bound, activated receptors, and this recognition promotes catalytic activation of GRKs, resulting in the preferential phosphorylation of activated receptors. GRK-phosphorylated receptors are then targeted by arrestin proteins, which bind to phosphorylated receptors. Arrestin-bound receptors are uncoupled from heterotrimeric G proteins, resulting in decreased sensitivity to further receptor stimulation (desensitization). Arrestin-bound receptors are also accelerated into internalization pathways and linked to distinct arrestin-mediated signaling pathways. GRKs thus serve as gatekeepers for receptors, terminating some signaling pathways and initiating others. One major outstanding question concerning GRKs understanding the mechanisms by which any particular receptor subtype (of the 800 or so in the body) is regulated by a specific GRK(s), and the consequences of this specificity. An understanding of this regulatory specificity could allow targeting of GRK function to ameliorate diseases involving GPCR dysregulation.
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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.