ArticleOncotarget2016
Schlafen2 mutation unravels a role for chronic ER stress in the loss of T cell quiescence.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Systemic Neurodegeneration and Brain Aging: Multi-Omics Disintegration, Proteostatic Collapse, and Network Failure Across the CNS.Biomedicines · 2025Review
- SLFN11-mediated tRNA regulation induces cell death by disrupting proteostasis in response to DNA-damaging agents.Nucleic acids research · 2025Article
- Unfolded protein responses in T cell immunity.Frontiers in immunology · 2024Review
- Integrated signaling and transcriptome analysis reveals Src family kinase individualities and novel pathways controlled by their constitutive activity.Frontiers in immunology · 2023Article
- Structural and biochemical characterization of human Schlafen 5.Nucleic acids research · 2022Article
- Review
- SLFN11 Inactivation Induces Proteotoxic Stress and Sensitizes Cancer Cells to Ubiquitin Activating Enzyme Inhibitor TAK-243.Cancer research · 2021Article
- SLFN2 protection of tRNAs from stress-induced cleavage is essential for T cell-mediated immunity.Science (New York, N.Y.) · 2021Article
- Stressed: The Unfolded Protein Response in T Cell Development, Activation, and Function.International journal of molecular sciences · 2019Review
- Survival of Naïve T Cells Requires the Expression of Let-7 miRNAs.Frontiers in immunology · 2019Article
- Interplay Between the Unfolded Protein Response and Immune Function in the Development of Neurodegenerative Diseases.Frontiers in immunology · 2018Review
- Slfn2 mutation-induced loss of T-cell quiescence leads to elevated de novo sterol synthesis.Immunology · 2017Article
- Endoplasmic reticulum stress regulates tumor growth and anti-tumor immunity: a promising opportunity for cancer immunotherapy.Cancer immunology, immunotherapy : CII · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunologically naïve lymphocytes are kept in a quiescent state until antigen engagement. These quiescent immune cells are characterized by small cell size, lack of spontaneous proliferation and low metabolic rate. Lymphocyte quiescence is actively enforced condition which ensures the preservation of proper differentiation and proliferation capabilities of naïve and memory lymphocytes. Previously we described a chemically induced mutation in Schlafen2 (Slfn2), termed elektra, which breaks quiescence and compromises immunity. However, the mechanism by which Slfn2 maintains quiescence remains unknown. Here we demonstrate that elektra T cells display chronic ER stress under steady state conditions. Modulation of ER stress response by depletion of either UPR mediators XBP1 or CHOP, improved viability and partially corrected the developmental abnormalities and proliferation capabilities of elektra T cells. Altogether, our results demonstrate a functional connection between Slfn2 induced quiescence in T cells and ER homeostasis, clarifying a novel mechanism by which immune cell quiescence is maintained.
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