ArticleFrontiers in immunology2018
SHIP1 Deficiency in Inflammatory Bowel Disease Is Associated With Severe Crohn's Disease and Peripheral T Cell Reduction.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Mast cell-derived IL-13 as a driver of Crohn disease-associated intestinal fibrosis.Inflammatory bowel diseases · 2026Article
- SHIP1 is required for T cell surveillance of occult malignancies.Cellular and molecular life sciences : CMLS · 2026Article
- Exploring putative links between gut microbiota and allergic rhinitis: insights from Mendelian randomization and multi-transcriptome integration.AMB Express · 2025Article
- The Inositol-5-Phosphatase SHIP1: Expression, Regulation and Role in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Review
- Aminocholestane and Aminoandrostane Inhibitors of the SH2 Domain-Containing Inositol 5'-Phosphatase (SHIP).ChemMedChem · 2025Article
- Functional Characterization of the SHIP1-Domains Regarding Their Contribution to Inositol 5-Phosphatase Activity.Biomolecules · 2025Article
- Environmental and inflammatory factors influencing concurrent gut and lung inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Ikaros sets the threshold for negative B-cell selection by regulation of the signaling strength of the AKT pathway.Cell communication and signaling : CCS · 2024Article
- The Functional Roles of the Src Homology 2 Domain-Containing Inositol 5-Phosphatases SHIP1 and SHIP2 in the Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- The relationship between extreme inter-individual variation in macrophage gene expression and genetic susceptibility to inflammatory bowel disease.Human genetics · 2024Article
- Functional characterization of Alzheimer's disease genetic variants in microglia.Nature genetics · 2023Article
- Null Function of Npr1 Disturbs Immune Response in Colonic Inflammation During Early Postnatal Stage.Inflammation · 2022Article
- Synthetic studies on the indane SHIP1 agonist AQX-1125.Organic & biomolecular chemistry · 2022Article
- Discovery of a novel SHIP1 agonist that promotes degradation of lipid-laden phagocytic cargo by microglia.iScience · 2022Article
- Targeting SHIP1 and SHIP2 in Cancer.Cancers · 2021Review
- SHIP-1, a target of miR-155, regulates endothelial cell responses in lung fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Integrated Bioinformatics Analysis Identifies ELAVL1 and APP as Candidate Crucial Genes for Crohn's Disease.Journal of immunology research · 2020Article
- Phosphatidylinositol 3-kinase p110δ drives intestinal fibrosis in SHIP deficiency.Mucosal immunology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
In our previous study, we observed a severe reduction in the Src homology 2-containing-inositol-phosphatase-1 (SHIP1) protein in a subpopulation of subjects from a small adult Crohn's Disease (CD) cohort. This pilot study had been undertaken since we had previously demonstrated that engineered deficiency of SHIP1 in mice results in a spontaneous and severe CD-like ileitis. Here, we extend our analysis of SHIP1 expression in peripheral blood mononuclear cells in a second much larger adult Inflammatory Bowel Disease (IBD) cohort, comprised of both CD and Ulcerative Colitis patients, to assess contribution of SHIP1 to the pathogenesis of human IBD. SHIP1 protein and mRNA levels were evaluated from blood samples obtained from IBD subjects seen at UCSF/SFVA, and compared to healthy control samples. Western blot analyses revealed that ~15% of the IBD subjects are severely SHIP1-deficient, with less than 10% of normal SHIP1 protein present in PBMC. Further analyses by flow cytometry and sequencing were performed on secondary samples obtained from the same subjects. Pan-hematolymphoid SHIP1 deficiency was a stable phenotype and was not due to coding changes in the
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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.