ArticleThe Journal of biological chemistry2010
Glucocorticoid-induced leucine zipper (GILZ) promotes the nuclear exclusion of FOXO3 in a Crm1-dependent manner.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Glucocorticoid-induced leucine zipper as a context-dependent central integrator of innate and adaptive immune homeostasis.Frontiers in immunology · 2026Review
- A coherent FOXO3-SNAI2 feed-forward loop in autophagy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Selinexor and the Selective Inhibition of Nuclear Export: A New Perspective on the Treatment of Sarcomas and Other Solid and Non-Solid Tumors.Pharmaceutics · 2021Review
- CDK4/6 regulate lysosome biogenesis through TFEB/TFE3.The Journal of cell biology · 2020Article
- Glucocorticoid-Induced Leucine Zipper: A Promising Marker for Monitoring and Treating Sepsis.Frontiers in immunology · 2020Review
- Implicating the Role of GILZ in Glucocorticoid Modulation of T-Cell Activation.Frontiers in immunology · 2019Review
- The Nuclear Export Inhibitor Selinexor Inhibits Hypoxia Signaling Pathways And 3D Spheroid Growth Of Cancer Cells.OncoTargets and therapy · 2019Article
- Glucocorticoid-Induced Leucine Zipper: A Novel Anti-inflammatory Molecule.Frontiers in pharmacology · 2019Review
- Transcription factors FOXO in the regulation of homeostatic hematopoiesis.Current opinion in hematology · 2018Review
- Glucocorticoid-Induced Leucine Zipper: Fine-Tuning of Dendritic Cells Function.Frontiers in immunology · 2018Review
- Selinexor (KPT-330) has antitumor activity against anaplastic thyroid carcinoma in vitro and in vivo and enhances sensitivity to doxorubicin.Scientific reports · 2017Article
- Molecular mechanism and therapeutic implications of selinexor (KPT-330) in liposarcoma.Oncotarget · 2017Article
- Neutrophil expression of glucocorticoid-induced leucine zipper (GILZ) anti-inflammatory protein is associated with acute respiratory distress syndrome severity.Annals of intensive care · 2016Article
- Glucocorticoid-Induced Leucine Zipper Is Expressed in Human Neutrophils and Promotes Apoptosis through Mcl-1 Down-Regulation.Journal of innate immunity · 2016Article
- Review
- Regulation of Bim in Health and Disease.Oncotarget · 2015Review
- GILZ as a Mediator of the Anti-Inflammatory Effects of Glucocorticoids.Frontiers in endocrinology · 2015Review
- XPO1 (CRM1) inhibition represses STAT3 activation to drive a survivin-dependent oncogenic switch in triple-negative breast cancer.Molecular cancer therapeutics · 2014Article
- Development of novel treatment strategies for inflammatory diseases-similarities and divergence between glucocorticoids and GILZ.Frontiers in pharmacology · 2014Review
- Upregulation of CRM1 relates to neuronal apoptosis after traumatic brain injury in adult rats.Journal of molecular neuroscience : MN · 2013Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GILZ (glucocorticoid-induced leucine zipper) is an ubiquitous protein whose expression is induced by glucocorticoids in lymphoid cells. We previously showed that GILZ expression is rapidly induced upon interleukin 2 deprivation in T-cells, protecting cells from apoptosis induced by forkhead box subgroup O3 (FOXO3). The aim of this work is to elucidate the molecular mechanism of FOXO factor inhibition by GILZ. We show in the myeloid cell line HL-60 and the lymphoid CTLL-2 T-cell line that GILZ down-regulates the expression of p27(KIP1) and Bim, two FOXO targets involved in cell cycle regulation and apoptosis, respectively. GILZ inhibits FOXO1, FOXO3, and FOXO4 transcriptional activities measured with natural or synthetic FOXO-responsive promoters in HL-60 cells. This inhibitory effect is independent of protein kinase B and IkappaB kinase phosphorylation sites. GILZ does not hinder FOXO3 DNA-binding activity and does not physically interact with FOXO3. However, using fluorescence microscopy, we observe that GILZ expression provokes a Crm-1-dependent nuclear exclusion of FOXO3 leading to its relocalization to the cytoplasm. Moreover, GILZ exclusive cytoplasmic localization is a prerequisite for FOXO3 inhibition and relocalization. We propose that GILZ is a general inhibitor of FOXO factors acting through an original mechanism by preventing them from reaching target genes within the nucleus.
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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.