ArticleBlood2009
SHIP is required for a functional hematopoietic stem cell niche.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed.
- SHIPi improves hematologic recovery after chemotherapy.Molecular medicine (Cambridge, Mass.) · 2025Article
- SHIP1 deficiency causes inflammation-dependent retardation in skeletal growth.Life science alliance · 2024Article
- A heterophil/lymphocyte-selected population reveals the phosphatase PTPRJ is associated with immune defense in chickens.Communications biology · 2023Article
- Hypoxia-Inducible Factors Signaling in Osteogenesis and Skeletal Repair.International journal of molecular sciences · 2022Review
- Lef1 ablation alleviates cartilage mineralization following posttraumatic osteoarthritis induction.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- SHIP1 Activator AQX-1125 Regulates Osteogenesis and Osteoclastogenesis Through PI3K/Akt and NF-κb Signaling.Frontiers in cell and developmental biology · 2022Article
- Targeting SHIP1 and SHIP2 in Cancer.Cancers · 2021Review
- Targeting PI3K/Akt/mTOR in AML: Rationale and Clinical Evidence.Journal of clinical medicine · 2020Review
- PI3K in stemness regulation: from development to cancer.Biochemical Society transactions · 2020Review
- Lipid phosphatase SHIP-1 regulates chondrocyte hypertrophy and skeletal development.Journal of cellular physiology · 2020Article
- Pan-SHIP1/2 inhibitors promote microglia effector functions essential for CNS homeostasis.Journal of cell science · 2020Article
- Loss of ENT1 increases cell proliferation in the annulus fibrosus of the intervertebral disc.Journal of cellular physiology · 2019Article
- Granulocyte-CSF links destructive inflammation and comorbidities in obstructive lung disease.The Journal of clinical investigation · 2018Article
- Regulation of Hematopoietic Cell Development and Function Through Phosphoinositides.Frontiers in immunology · 2018Review
- Alzheimer's Disease: From Genetic Variants to the Distinct Pathological Mechanisms.Frontiers in molecular neuroscience · 2017Review
- A small-molecule inhibitor of SHIP1 reverses age- and diet-associated obesity and metabolic syndrome.JCI insight · 2016Article
- Synthesis and initial evaluation of quinoline-based inhibitors of the SH2-containing inositol 5'-phosphatase (SHIP).Bioorganic & medicinal chemistry letters · 2015Article
- Role of SHIP1 in Invariant NKT Cell Development and Functions.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- IL-33 signaling contributes to the pathogenesis of myeloproliferative neoplasms.The Journal of clinical investigation · 2015Article
- SHIP1-expressing mesenchymal stem cells regulate hematopoietic stem cell homeostasis and lineage commitment during aging.Stem cells and development · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
SH2-domain-containing inositol 5'-phosphatase-1 (SHIP) deficiency significantly increases the number of hematopoietic stem cells (HSCs) present in the bone marrow (BM). However, the reconstitution capacity of these HSCs is severely impaired, suggesting that SHIP expression might be an intrinsic requirement for HSC function. To further examine this question, we developed a model in which SHIP expression is ablated in HSCs while they are resident in a SHIP-competent milieu. In this setting, we find that long-term repopulation by SHIP-deficient HSCs is not compromised. Moreover, SHIP-deficient HSCs from this model repopulate at levels comparable with wild-type HSCs upon serial transfer. However, when HSCs from mice with systemic ablation of SHIP are transplanted, they are functionally compromised for repopulation. These findings demonstrate that SHIP is not an intrinsic requirement for HSC function, but rather that SHIP is required for the BM milieu to support functionally competent HSCs. Consistent with these findings, cells that comprise the BM niche express SHIP and SHIP deficiency profoundly alters their function.
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What OpenQuestion holds
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.