ArticleEndocrine2003
Differential expression of GRK isoforms in nonmalignant and malignant human granulosa cells.
Article in Endocrine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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
15 citing papers in PubMed, 42 citations in OpenAlex.
- G-protein coupled receptor kinase-2 regulates the migration of chronic lymphocytic leukaemia cells to sphingosine-1 phosphate in vitro and their trafficking in vivo.Scientific reports · 2025Article
- Quantitative proteomics assay reveals G protein-coupled receptor kinase 4-induced HepG2 cell growth inhibition.Heliyon · 2024Article
- Review
- Transcriptome signatures of host tissue infected with African swine fever virus reveal differential expression of associated oncogenes.Archives of virology · 2024Review
- Interactions between AT1R and GRKs: the determinants for activation of signaling pathways involved in blood pressure regulation.Molecular biology reports · 2023Review
- G Protein-Coupled Receptor Kinase 4 Is a Novel Prognostic Factor in Hepatocellular Carcinoma.Disease markers · 2022Article
- The GRKs Reactome: Role in Cell Biology and Pathology.International journal of molecular sciences · 2021Review
- The role of G protein-coupled receptor kinases in the pathology of malignant tumors.Acta pharmacologica Sinica · 2018Review
- The Role of G Protein-coupled Receptor Kinases in Cancer.International journal of biological sciences · 2018Review
- G Protein-Coupled Receptor Kinases in the Inflammatory Response and Signaling.Advances in immunology · 2017Review
- Adrenergic signaling in heart failure and cardiovascular aging.Maturitas · 2016Review
- G Protein Coupled Receptor Kinase 3 Regulates Breast Cancer Migration, Invasion, and Metastasis.PloS one · 2016Article
- G protein-coupled receptor kinase 2 (GRK2) is localized to centrosomes and mediates epidermal growth factor-promoted centrosomal separation.Molecular biology of the cell · 2013Article
- G-protein-coupled receptor kinase 2 and hypertension: molecular insights and pathophysiological mechanisms.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2013Review
- Mdm2 is involved in the ubiquitination and degradation of G-protein-coupled receptor kinase 2.The EMBO journal · 2006Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Granulosa cell tumors are serious ovarian neoplasms that can occur in women of all ages. While there have been numerous attempts to understand the cause of these malignancies, the pathogenesis of granulosa cell tumors (GCTs) still remains largely unknown. G-protein coupled receptor kinases (GRKs) are important regulators of signal transduction through the process of receptor desensitization and internalization. Receptors that are regulated by GRKs are members of the large family of seven-transmembrane receptors and include the follicle stimulating hormone receptor (FSHR). In granulosa cells, the FSH signaling system is responsible for cell proliferation, differentiation, and steroidogenesis. In the studies presented, we examined GRK mRNA and protein expression in nonmalignant human granulosa cells, in KGN cells, a human GCT cell line, and in a panel of human GCT samples. The KGN tumor cells express significantly less GRK4 alpha/beta protein and higher levels of GRK2 and GRK4 gamma/delta protein as compared to nonmalignant human granulosa cells. In human GCT samples, GRK4 alpha/beta protein was detected in 3 of the 13 tumor samples, whereas gamma/delta proteins expression was detected in all samples. These findings suggest that GRK protein expression is altered in GCTs and may be involved in the pathogenesis of these tumors.
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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.