ArticleThe Journal of cell biology2005
Cytokine-driven cell cycling is mediated through Cdc25A.
Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 65 citations in OpenAlex.
- EpoR stimulates rapid cycling and larger red cells during mouse and human erythropoiesis.Nature communications · 2021Trial
- Autophagy and Cancer Dormancy.Frontiers in oncology · 2021Review
- Article
- Critical reanalysis of the methods that discriminate the activity of CDK2 from CDK1.Cell cycle (Georgetown, Tex.) · 2016Review
- Targeting Homeostatic T Cell Proliferation to Control Beta-Cell Autoimmunity.Current diabetes reports · 2016Review
- Telekin suppresses human hepatocellular carcinoma cells in vitro by inducing G2/M phase arrest via the p38 MAPK signaling pathway.Acta pharmacologica Sinica · 2014Article
- S-adenosylmethionine limitation induces p38 mitogen-activated protein kinase and triggers cell cycle arrest in G1.Journal of cell science · 2014Article
- PD-1 inhibits T cell proliferation by upregulating p27 and p15 and suppressing Cdc25A.Cell cycle (Georgetown, Tex.) · 2012Article
- The major isoforms of Bim contribute to distinct biological activities that govern the processes of autophagy and apoptosis in interleukin-7 dependent lymphocytes.Biochimica et biophysica acta · 2012Article
- Selective effects of PD-1 on Akt and Ras pathways regulate molecular components of the cell cycle and inhibit T cell proliferation.Science signaling · 2012Article
- JunD/AP-1-mediated gene expression promotes lymphocyte growth dependent on interleukin-7 signal transduction.PloS one · 2012Article
- CDC25A(Q110del): a novel cell division cycle 25A isoform aberrantly expressed in non-small cell lung cancer.PloS one · 2012Article
- Seeing is believing: illuminating the source of in vivo interleukin-7.Immune network · 2011Article
- Cdc25A-driven proliferation regulates CD62L levels and lymphocyte movement in response to interleukin-7.Experimental hematology · 2010Article
- Increased CD4+ T cell levels during IL-7 administration of antiretroviral therapy-treated simian immunodeficiency virus-positive macaques are not dependent on strong proliferative responses.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- The interaction of LCK and the CD4 co-receptor alters the dose response of T-cells to interleukin-7.Immunology letters · 2010Article
- Interleukin-7 mediates glucose utilization in lymphocytes through transcriptional regulation of the hexokinase II gene.American journal of physiology. Cell physiology · 2010Article
- Interleukin-7 regulates Bim proapoptotic activity in peripheral T-cell survival.Molecular and cellular biology · 2010Article
- CRP identifies homeostatic immune oscillations in cancer patients: a potential treatment targeting tool?Journal of translational medicine · 2009Review
- The extracellular signal-regulated kinase-mitogen-activated protein kinase pathway phosphorylates and targets Cdc25A for SCF beta-TrCP-dependent degradation for cell cycle arrest.Molecular biology of the cell · 2009Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Lymphocytes are the central mediators of the immune response, requiring cytokines for survival and proliferation. Survival signaling targets the Bcl-2 family of apoptotic mediators, however, the pathway for the cytokine-driven proliferation of lymphocytes is poorly understood. Here we show that cytokine-induced cell cycle progression is not solely dependent on the synthesis of cyclin-dependent kinases (Cdks) or cyclins. Rather, we observe that in lymphocyte cell lines dependent on interleukin-3 or interleukin-7, or primary lymphocytes dependent on interleukin 7, the phosphatase Cdc25A is the critical mediator of proliferation. Withdrawal of IL-7 or IL-3 from dependent lymphocytes activates the stress kinase, p38 MAPK, which phosphorylates Cdc25A, inducing its degradation. As a result, Cdk/cyclin complexes remain phosphorylated and inactive and cells arrest before the induction of apoptosis. Inhibiting p38 MAPK or expressing a mutant Cdc25A, in which the two p38 MAPK target sites, S75 and S123, are altered, renders cells resistant to cytokine withdrawal, restoring the activity of Cdk/cyclin complexes and driving the cell cycle independent of a growth stimulus.
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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.