ArticleImmunology2002
Insulin-like growth factor-1 activates Akt and Jun N-terminal kinases (JNKs) in promoting the survival of T lymphocytes.
Article in Immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 69 citations in OpenAlex.
- Article
- Insulin-like growth factor-1 receptor crosstalk with integrins, cadherins, and the tumor microenvironment: sticking points in understanding IGF1R function in cancer.Endocrine-related cancer · 2023Review
- Insulin-like Growth Factor-1 Synergizes with IL-2 to Induce Homeostatic Proliferation of Regulatory T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Senescent alveolar macrophages promote early-stage lung tumorigenesis.Cancer cell · 2023Article
- Targeting Insulin-Like Growth Factor-I in Management of Neurological Disorders.Neurotoxicity research · 2022Review
- Serum IGF-1 in patients with rheumatoid arthritis: correlation with disease activity.BMC research notes · 2022Article
- Correlation of Plasma Level of Insulin-Like Growth Factor-1 (IGF-1) with Bacterial Index on Leprosy Patients in Bali.Annals of dermatology · 2020Article
- IGF1R Axis Inhibition Restores Dendritic Cell Antitumor Response in Ovarian Cancer.Translational oncology · 2020Article
- Associations betweenAnimals : an open access journal from MDPI · 2020Article
- Role of Insulin-Like Growth Factor Binding Protein-3 in the Pathogenesis of Herpes Stromal Keratitis.Investigative ophthalmology & visual science · 2020Article
- A Novel Mutation in Insulin-Like Growth Factor 1 Receptor (c.641-2A>G) Is Associated with Impaired Growth, Hypoglycemia, and Modified Immune Phenotypes.Hormone research in paediatrics · 2020Article
- High Expression of STAT3 in Subcutaneous Adipose Tissue Associates with Cardiovascular Risk in Women with Rheumatoid Arthritis.International journal of molecular sciences · 2017Article
- Uromodulin p.Cys147Trp mutation drives kidney disease by activating ER stress and apoptosis.The Journal of clinical investigation · 2017Article
- Insulin-Like Growth Factor-1 Deficiency and Cirrhosis Establishment.Journal of clinical medicine research · 2017Review
- Insulin and Insulin-like growth factor-1 can activate the phosphoinositide-3-kinase /Akt/FoxO1 pathway in T cellsDermato-endocrinology · 2017Article
- Lack of AKT in adipocytes causes severe lipodystrophy.Molecular metabolism · 2016Article
- Mitochondria-derived hydrogen peroxide selectively enhances T cell receptor-initiated signal transduction.The Journal of biological chemistry · 2013Article
- Burn injury induces high levels of phosphorylated insulin-like growth factor binding protein-1.International journal of burns and trauma · 2013Article
- Human conditions of insulin-like growth factor-I (IGF-I) deficiency.Journal of translational medicine · 2012Review
- Inhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant chronic myeloid leukaemia cells.Journal of cellular and molecular medicine · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin-like growth factor 1 receptor (IGF-1R) expression is augmented on T cells upon ligation of CD28, and this promotes IGF-1-mediated protection from Fas-induced cell death for up to 6 days. To determine the mechanism of action of IGF-1R in T-cell expansion, we investigated the signalling pathways activated by IGF-1 in T cells and in Jurkat cells. We found that IGF-1 transiently induces Akt, jun N-terminal kinases (JNK), and c-Jun phosphorylation in activated T cells, with JNK and c-Jun phosphorylation occurring faster than Akt phosphorylation. To mimic IGF-1R expression levels in CD28-stimulated Jurkat cells these cells were stably transfected to over-express the IGF-1R. Jurkat/IGF-1R cells exhibited enhanced constitutive Akt phosphorylation compared with mock-transfected controls, but IGF-1 induced transient phosphorylation of MKK4, JNKs, and c-Jun. Inhibition of PI-3 kinase activity and Akt phosphorylation with LY294002 totally suppressed IGF-1-mediated protection from Fas killing in activated T cells, but only partially suppressed IGF-1-mediated protection in Jurkat/IGF-1R cells. However, either dicumarol in T cells or a dominant negative JNK1 (APF) in Jurkat/IGF-1R cells greatly suppressed IGF-1-mediated protection from Fas killing. Together, these data demonstrate that IGF-1-mediated activation of JNKs and PI-3 kinase contributes to normal T-cell survival, whereas the JNK pathway may be more important in Jurkat leukaemia cells.
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