ArticleThe Journal of clinical investigation1995
Regulation of G protein-coupled receptor kinase subtypes in activated T lymphocytes. Selective increase of beta-adrenergic receptor kinase 1 and 2.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 113 citations in OpenAlex.
- DNA methylation and whole-genome transcription analysis in CD4Clinical epigenetics · 2024Article
- Review
- G protein-coupled receptor kinase 2 (GRK2) as a multifunctional signaling hub.Cellular and molecular life sciences : CMLS · 2019Review
- GRK2 mediates TCR-induced transactivation of CXCR4 and TCR-CXCR4 complex formation that drives PI3Kγ/PREX1 signaling and T cell cytokine secretion.The Journal of biological chemistry · 2018Article
- Sympathetic Nerve Hyperactivity in the Spleen: Causal for Nonpathogenic-Driven Chronic Immune-Mediated Inflammatory Diseases (IMIDs)?International journal of molecular sciences · 2018Review
- Noncanonical Roles of G Protein-coupled Receptor Kinases in Cardiovascular Signaling.Journal of cardiovascular pharmacology · 2017Review
- Non-redundant requirement for CXCR3 signalling during tumoricidal T-cell trafficking across tumour vascular checkpoints.Nature communications · 2015Article
- The evolving impact of g protein-coupled receptor kinases in cardiac health and disease.Physiological reviews · 2015Review
- Molecular mechanisms underlying β-adrenergic receptor-mediated cross-talk between sympathetic neurons and immune cells.International journal of molecular sciences · 2015Review
- Neuronal NF1/RAS regulation of cyclic AMP requires atypical PKC activation.Human molecular genetics · 2014Article
- Prostaglandin E2 affects T cell responses through modulation of CD46 expression.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Migration of Th1 lymphocytes is regulated by CD152 (CTLA-4)-mediated signaling via PI3 kinase-dependent Akt activation.PloS one · 2012Article
- Myeloid-specific GPCR kinase-2 negatively regulates NF-κB1p105-ERK pathway and limits endotoxemic shock in mice.Journal of cellular physiology · 2011Article
- Neural pathways in allergic inflammation.Journal of allergy · 2010Article
- Granulocyte chemotaxis and disease expression are differentially regulated by GRK subtype in an acute inflammatory arthritis model (K/BxN).Clinical immunology (Orlando, Fla.) · 2008Article
- Leukocyte analysis from WHIM syndrome patients reveals a pivotal role for GRK3 in CXCR4 signaling.The Journal of clinical investigation · 2008Article
- G protein-coupled receptor kinase 2 negatively regulates chemokine signaling at a level downstream from G protein subunits.Molecular biology of the cell · 2006Article
- Once and future signaling: G protein-coupled receptor kinase control of neuronal sensitivity.Neuromolecular medicine · 2005Review
- Glucocorticoids reverse IL-1beta-induced impairment of beta-adrenoceptor-mediated relaxation and up-regulation of G-protein-coupled receptor kinases.British journal of pharmacology · 2002Article
- G-protein-coupled receptor kinase activity is increased in hypertension.The Journal of clinical investigation · 1997Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Beta-adrenergic receptor kinase (beta ARK) is a serine-threonine kinase involved in the process of homologous desensitization of G-coupled receptors. beta ARK is a member of a multigene family, consisting of six known subtypes, also named G protein-coupled receptor kinases (GRK 1-6). In this study we investigated the expression of GRKs during the process of T cell activation, which is of fundamental importance in regulating immune responses. T cell activation was induced by exposing mononuclear leukocytes (MNL) to PHA and confirmed by tritiated thymidine incorporation measurement. A substantial increase of GRK activity (as measured by in vitro phosphorylation of rhodopsin) was found after 48 h (331 +/- 80% of controls) and 72 h (347 +/- 86% of controls) of exposure to PHA. A threefold increase of beta ARK1 immunoreactivity was found in MNL exposed to PHA for 72 h. Persistent activation of protein kinase C (PKC) by 10 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) was able to increase beta ARK activity to the same extent as PHA, suggesting a PKC-mediated mechanism. The kinetic of beta-adrenergic-stimulated cAMP production was substantially modified in TPA and PHA-activated cells, indicating that the increased GRK activity resulted in an increased beta-adrenergic homologous desensitization. A three- to fourfold increase in GRK activity was also observed in a population of T cell blasts (> 97% CD3+) exposed to PHA for 48-72 h. A significant increase in beta ARK1 and beta ARK2 mRNA expression was observed 48 h after mitogen stimulation, while mRNA expression of GRK5 and GRK6 was not changed. In conclusion our data show that the expression of GRK subtypes is actively and selectively modulated according to the functional state of T lymphocytes.
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