ArticleMolecular endocrinology (Baltimore, Md.)2011
Glucocorticoid receptor alpha isoform-selective regulation of antiapoptotic genes in osteosarcoma cells: a new mechanism for glucocorticoid resistance.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed, 54 citations in OpenAlex.
- Levonorgestrel-induced modulation of triple negative breast cancer proliferation via glucocorticoid receptor.3 Biotech · 2025Article
- Perinatal glucocorticoid sensitivity in the preterm newborn: molecular mechanisms, endogenous determinants, and clinical implications.Frontiers in endocrinology · 2025Review
- The Glucocorticoid Receptor: Isoforms, Functions, and Contribution to Glucocorticoid Sensitivity.Endocrine reviews · 2024Review
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Corticosterone and Glucocorticoid Receptor in the Cortex of Rats during Aging-The Effects of Long-Term Food Restriction.Nutrients · 2021Article
- Glucocorticoid therapy in assisted reproduction.Clinical and experimental reproductive medicine · 2021Article
- Conserved allosteric ensembles in disordered proteins using TROSY/anti-TROSY RBiophysical journal · 2021Article
- A multifunctional dexamethasone-delivery implant fabricated using atmospheric plasma and its effects on apoptosis, osteogenesis and inflammation.Drug delivery and translational research · 2021Article
- Therapeutic targeting of pancreatic cancer stem cells by dexamethasone modulation of the MKP-1-JNK axis.The Journal of biological chemistry · 2020Article
- Glucocorticoid Receptor Mutations and Hypersensitivity to Endogenous and Exogenous Glucocorticoids.The Journal of clinical endocrinology and metabolism · 2018Article
- Glucocorticoids and Reproduction: Traffic Control on the Road to Reproduction.Trends in endocrinology and metabolism: TEM · 2017Review
- The effects of microRNAs on glucocorticoid responsiveness.Journal of cancer research and clinical oncology · 2017Review
- Gene expression profiling of tumor-initiating stem cells from mouse Krebs-2 carcinoma using a novel marker of poorly differentiated cells.Oncotarget · 2017Article
- Glucocorticoid-induced tethered transrepression requires SUMOylation of GR and formation of a SUMO-SMRT/NCoR1-HDAC3 repressing complex.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- GR SUMOylation and formation of an SUMO-SMRT/NCoR1-HDAC3 repressing complex is mandatory for GC-induced IR nGRE-mediated transrepression.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Corticosteroids: Mechanisms of Action in Health and Disease.Rheumatic diseases clinics of North America · 2016Review
- Specificity and sensitivity of glucocorticoid signaling in health and disease.Best practice & research. Clinical endocrinology & metabolism · 2015Review
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- HES1 is a master regulator of glucocorticoid receptor-dependent gene expression.Science signaling · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Glucocorticoids regulate a variety of physiological processes and are commonly used to treat disorders of inflammation, autoimmune diseases, and cancer. Glucocorticoid action is predominantly mediated through the classic glucocorticoid receptor (GR)α isoform. Recent data suggest that the mature GRα mRNA is translated into multiple N-terminal isoforms that have distinct biochemical properties and gene regulatory profiles. Interestingly, osteosarcoma cells stably expressing the GRα-D translational isoform are unique in that they are resistant to glucocorticoid-induced apoptosis. In this study, we investigate whether GRα isoform-specific differences in the regulation of antiapoptotic genes contribute to this resistant phenotype. We now show that GRα-D, unlike the other receptor isoforms, does not inhibit the activity of a nuclear factor κB (NF-κB)-responsive reporter gene and does not efficiently repress either the transcription or protein production of the antiapoptotic genes Bcl-xL, cellular inhibitor of apoptosis protein 1, and survivin. The inability of GRα-D to down-regulate the expression of these genes appears to be associated with a diminished interaction between GRα-D and NF-κB that is observed in cells, but not in vitro, and likely reflects the sequestration of GRα-D in the nucleus. Deletion of the GRα N-terminal amino acids 98-335 also results in a nuclear resident GR, which fails to interact with NF-κB in cells and promote apoptosis in response to glucocorticoids. These data suggest that the N-terminal translational isoforms of GRα selectively regulate antiapoptotic genes and that the GRα-D isoform may contribute to the resistance of certain cancer cells to glucocorticoid-induced apoptosis.
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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.