ArticleFEBS letters2013
Mitochondrial G protein coupled receptor kinase 2 regulates proinflammatory responses in macrophages.
Article in FEBS letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 40 citations in OpenAlex.
- Pharmacological inhibition of G protein-coupled receptor kinase 2 (GRK2) by paroxetine attenuates acetaminophen-induced hepatotoxicity.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Cys340Ser Mutation Abolishing S-Nitrosylation Drives GRK2 Mitochondrial Localization and Dysfunction.Cells · 2026Article
- Mitochondrial accumulation of GRK2 as a protective mechanism against hypoxia-induced endothelial dysfunction.Cell death discovery · 2025Article
- GRK2 and Mitochondrial Dynamics in Cardiovascular Health and Disease.International journal of molecular sciences · 2025Review
- Canonical or non-canonical, all aspects of G protein-coupled receptor kinase 2 in heart failure.Acta physiologica (Oxford, England) · 2025Review
- Unveiling the Role of GRK2: From Immune Regulation to Cancer Therapeutics.Mediators of inflammation · 2025Review
- Infiltrating macrophages amplify doxorubicin-induced cardiac damage: role of catecholamines.Cellular and molecular life sciences : CMLS · 2023Article
- PEBP balances apoptosis and autophagy in whitefly upon arbovirus infection.Nature communications · 2022Article
- G protein-coupled receptor kinase 2 modifies the cellular reaction to cisplatin through interactions with NADPH oxidase 4.Molecular and cellular biochemistry · 2021Article
- Review
- Article
- Role of Endothelial G Protein-Coupled Receptor Kinase 2 in Angioedema.Hypertension (Dallas, Tex. : 1979) · 2020Article
- G protein-coupled receptor kinase 2 (GRK2) as a multifunctional signaling hub.Cellular and molecular life sciences : CMLS · 2019Review
- G protein-coupled receptor kinase 2 regulates mitochondrial bioenergetics and impairs myostatin-mediated autophagy in muscle cells.American journal of physiology. Cell physiology · 2019Article
- NFkappaB is a Key Player in the Crosstalk between Inflammation and Cardiovascular Diseases.International journal of molecular sciences · 2019Review
- Antidiabetic and Cardioprotective Effects of Pharmacological Inhibition of GRK2 in db/db Mice.International journal of molecular sciences · 2019Article
- GRKs and β-Arrestins: "Gatekeepers" of Mitochondrial Function in the Failing Heart.Frontiers in pharmacology · 2019Review
- G protein-coupled receptor kinase-2-deficient mice are protected from dextran sodium sulfate-induced acute colitis.Physiological genomics · 2018Article
- GPCR desensitization: Acute and prolonged phases.Cellular signalling · 2018Review
- A Novel Small Peptide Inhibitor of NFOxidative medicine and cellular longevity · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
G-protein-coupled receptor kinase 2 (GRK2) levels are elevated in inflammation but its role is not clear yet. Here we show that GRK2 expression is dependent on NFκB transcriptional activity. In macrophages, LPS induces GRK2 accumulation in mitochondria increasing biogenesis. The overexpression of the carboxy-terminal domain of GRK2 (βARK-ct), known to displace GRK2 from plasma membranes, induces earlier localization of GRK2 to mitochondria in response to LPS leading to increased mt-DNA transcription and reduced ROS production and cytokine expression. Our study shows the relevance of GRK2 subcellular localization in macrophage biology and its potential therapeutic properties in inflammation.
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.