ArticleLeukemia2010
SHIP-1 inhibits CD95/APO-1/Fas-induced apoptosis in primary T lymphocytes and T leukemic cells by promoting CD95 glycosylation independently of its phosphatase activity.
Article in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 47 citations in OpenAlex.
- Multifaceted roles of Galectins: from carbohydrate binding to targeted cancer therapy.Biomarker research · 2025Review
- Glycosylation: mechanisms, biological functions and clinical implications.Signal transduction and targeted therapy · 2024Review
- Galectin-9 in Gastroenterological Cancer.International journal of molecular sciences · 2023Review
- Doxycycline Significantly Enhances Induction of Induced Pluripotent Stem Cells to Endoderm by Enhancing Survival Through Protein Kinase B Phosphorylation.Hepatology (Baltimore, Md.) · 2021Article
- Role of Glycans on Key Cell Surface Receptors That Regulate Cell Proliferation and Cell Death.Cells · 2021Review
- Targeting SHIP1 and SHIP2 in Cancer.Cancers · 2021Review
- Receptor Oligomerization and Its Relevance for Signaling by Receptors of the Tumor Necrosis Factor Receptor Superfamily.Frontiers in cell and developmental biology · 2020Review
- Decoding the sweet regulation of apoptosis: the role of glycosylation and galectins in apoptotic signaling pathways.Cell death and differentiation · 2019Review
- The impact of phosphoinositide 5-phosphatases on phosphoinositides in cell function and human disease.Journal of lipid research · 2019Review
- A Drosophila Tumor Suppressor Gene Prevents Tonic TNF Signaling through Receptor N-Glycosylation.Developmental cell · 2018Article
- N-glycosylation of mouse TRAIL-R restrains TRAIL-induced apoptosis.Cell death & disease · 2018Article
- Multiple Roles of Glycans in Hematological Malignancies.Frontiers in oncology · 2018Review
- Tissue Inhibitor of Metalloproteinase-3 (TIMP-3) induces FAS dependent apoptosis in human vascular smooth muscle cells.PloS one · 2018Article
- Cancer Therapy Due to Apoptosis: Galectin-9.International journal of molecular sciences · 2017Review
- Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis.International journal of molecular sciences · 2016Review
- Impaired T-cell survival promotes mucosal inflammatory disease in SHIP1-deficient mice.Mucosal immunology · 2014Article
- Role of inositol poly-phosphatases and their targets in T cell biology.Frontiers in immunology · 2013Review
- Glycobiology of cell death: when glycans and lectins govern cell fate.Cell death and differentiation · 2013Review
- Aberrant O-glycosylation and anti-glycan antibodies in an autoimmune disease IgA nephropathy and breast adenocarcinoma.Cellular and molecular life sciences : CMLS · 2013Review
- Role of SHIP1 in cancer and mucosal inflammation.Annals of the New York Academy of Sciences · 2013Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
SHIP-1 (SH2 (Src homology 2)-containing inositol 5'-phosphatase-1) functions as a negative regulator of immune responses by hydrolyzing phosphatidylinositol-3,4,5-triphosphate generated by phosphoinositide-3 (PI 3)-kinase activity. As a result, SHIP-1 deficiency in mice results in myeloproliferation and B-cell lymphoma. On the other hand, SHIP-1-deficient mice have a reduced T-cell population, but the underlying mechanisms are unknown. In this work, we hypothesized that SHIP-1 plays anti-apoptotic functions in T cells upon stimulation of the death receptor CD95/APO-1/Fas. Using primary T cells from SHIP-1(-/-) mice and T leukemic cell lines, we report that SHIP-1 is a potent inhibitor of CD95-induced death. We observed that a small fraction of the SHIP-1 pool is localized to the endoplasmic reticulum (ER), in which it promotes CD95 glycosylation. This post-translational modification requires an intact SH2 domain of SHIP-1, but is independent of its phosphatase activity. The glycosylated CD95 fails to oligomerize upon stimulation, resulting in impaired death-inducing signaling complex (DISC) formation and downstream apoptotic cascade. These results uncover an unanticipated inhibitory function for SHIP-1 and emphasize the role of glycosylation in the regulation of CD95 signaling in T cells. This work may also provide a new basis for therapeutic strategies using compounds inducing apoptosis through the CD95 pathway on SHIP-1-negative leukemic T cells.
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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 Socratic graph.