ArticleBMC genomics2009
Molecular signature of cell cycle exit induced in human T lymphoblasts by IL-2 withdrawal.
Article in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Human Epididymis Secretory Protein 4 (HE4) Compromises Cytotoxic Mononuclear Cells via Inducing Dual Specificity Phosphatase 6.Frontiers in pharmacology · 2019Article
- Slfn2 mutation-induced loss of T-cell quiescence leads to elevated de novo sterol synthesis.Immunology · 2017Article
- Loss of T-cell quiescence by targeting Slfn2 prevents the development and progression of T-ALL.Oncotarget · 2016Article
- Schlafen2 mutation unravels a role for chronic ER stress in the loss of T cell quiescence.Oncotarget · 2016Article
- Four genetic variants interact to confer susceptibility to atopic dermatitis in Chinese Han population.Molecular genetics and genomics : MGG · 2015Article
- Elevated C1orf63 expression is correlated with CDK10 and predicts better outcome for advanced breast cancers: a retrospective study.BMC cancer · 2015Article
- Identification of epigenetic modifications that contribute to pathogenesis in therapy-related AML: Effective integration of genome-wide histone modification with transcriptional profiles.BMC medical genomics · 2015Article
- Epigenetic basis of regeneration: analysis of genomic DNA methylation profiles in the MRL/MpJ mouse.DNA research : an international journal for rapid publication of reports on genes and genomes · 2013Article
- Profiling of autoantibodies in IgA nephropathy, an integrative antibiomics approach.Clinical journal of the American Society of Nephrology : CJASN · 2011Article
- An Slfn2 mutation causes lymphoid and myeloid immunodeficiency due to loss of immune cell quiescence.Nature immunology · 2010Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe molecular mechanisms of cell cycle exit are poorly understood. Studies on lymphocytes at cell cycle exit after growth factor deprivation have predominantly focused on the initiation of apoptosis. We aimed to study gene expression profile of primary and immortalised IL-2-dependent human T cells forced to exit the cell cycle by growth factor withdrawal, before apoptosis could be evidenced.
resultsBy the Affymetrix microarrays HG-U133 2.0 Plus, 53 genes were distinguished as differentially expressed before and soon after IL-2 deprivation. Among those, PIM1, BCL2, IL-8, HBEGF, DUSP6, OSM, CISH, SOCS2, SOCS3, LIF and IL13 were down-regulated and RPS24, SQSTM1, TMEM1, LRRC8D, ECOP, YY1AP1, C1orf63, ASAH1, SLC25A46 and MIA3 were up-regulated. Genes linked to transcription, cell cycle, cell growth, proliferation and differentiation, cell adhesion, and immune functions were found to be overrepresented within the set of the differentially expressed genes.
conclusionCell cycle exit of the growth factor-deprived T lymphocytes is characterised by a signature of differentially expressed genes. A coordinate repression of a set of genes known to be induced during T cell activation is observed. However, growth arrest following exit from the cell cycle is actively controlled by several up-regulated genes that enforce the non-dividing state. The identification of genes involved in cell cycle exit and quiescence provides new hints for further studies on the molecular mechanisms regulating the non-dividing state of a cell, the mechanisms closely related to cancer development and to many biological processes.
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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.