ArticleThe Journal of clinical investigation1999
Altered responsiveness to chemokines due to targeted disruption of SHIP.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
32 citing papers in PubMed, 99 citations in OpenAlex.
- Review
- CXCL15/Lungkine has suppressive activity on proliferation and expansion of multi-potential, erythroid, granulocyte and macrophage progenitors in S-phase specific manner.Blood cells, molecules & diseases · 2021Article
- MicroRNA-155 promotes G-CSF-induced mobilization of murine hematopoietic stem and progenitor cells via propagation of CXCL12 signaling.Leukemia · 2017Article
- Modulation of Hematopoietic Chemokine Effects In Vitro and In Vivo by DPP-4/CD26.Stem cells and development · 2016Article
- SHIP represses lung inflammation and inhibits mammary tumor metastasis in BALB/c mice.Oncotarget · 2016Article
- SHIP1-expressing mesenchymal stem cells regulate hematopoietic stem cell homeostasis and lineage commitment during aging.Stem cells and development · 2015Article
- CXCL12/CXCR4 axis in the pathogenesis of acute lymphoblastic leukemia (ALL): a possible therapeutic target.Cellular and molecular life sciences : CMLS · 2015Review
- Negative regulation of chemokine receptor signaling and B-cell chemotaxis by p66Shc.Cell death & disease · 2014Article
- Role of inositol poly-phosphatases and their targets in T cell biology.Frontiers in immunology · 2013Review
- CXCL12 induces hepatic stellate cell contraction through a calcium-independent pathway.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Characterization of AQX-1125, a small-molecule SHIP1 activator: Part 1. Effects on inflammatory cell activation and chemotaxis in vitro and pharmacokinetic characterization in vivo.British journal of pharmacology · 2013Article
- Characterization of AQX-1125, a small-molecule SHIP1 activator: Part 2. Efficacy studies in allergic and pulmonary inflammation models in vivo.British journal of pharmacology · 2013Article
- Role of inositol phospholipid signaling in natural killer cell biology.Frontiers in immunology · 2013Article
- A mutation in synaptojanin 2 causes progressive hearing loss in the ENU-mutagenised mouse strain Mozart.PloS one · 2011Article
- Inositol phospholipid signaling and the biology of natural killer cells.Journal of innate immunity · 2011Review
- Article
- Survival of monocytes and macrophages and their role in health and disease.Frontiers in bioscience (Landmark edition) · 2009Review
- The inositol phosphatase SHIP controls Salmonella enterica serovar Typhimurium infection in vivo.Infection and immunity · 2008Article
- Article
- Phosphoinositide phosphatases in a network of signalling reactions.Pflugers Archiv : European journal of physiology · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
SHIP has been implicated in negative signaling in a number of hematopoietic cell types and is postulated to downregulate phosphatidylinositol-3-kinase- (PI-3K-) initiated events in diverse receptor signaling pathways. Because PI-3K is implicated in chemokine signaling, we investigated whether SHIP plays any role in cellular responses to chemokines. We found that a number of immature and mature hematopoietic cells from SHIP-deficient mice manifested enhanced directional migration (chemotaxis) in response to the chemokines stromal cell-derived factor-1 (SDF-1) and B-lymphocyte chemoattractant (BLC). SHIP(-/-) cells were also more active in calcium influx and actin polymerization in response to SDF-1. However, colony formation by SHIP-deficient hematopoietic progenitor cell (HPCs) was not inhibited by 13 myelosuppressive chemokines that normally inhibit proliferation of HPCs. These altered biologic activities of chemokines on SHIP-deficient cells are not caused by simple modulation of chemokine receptor expression in SHIP-deficient mice, implicating SHIP in the modulation of chemokine-induced signaling and downstream effects.
Indexed as
Identifiers
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.