ReviewAnnals of the New York Academy of Sciences2013
Role of SHIP1 in cancer and mucosal inflammation.
Review in Annals of the New York Academy of Sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 40 citations in OpenAlex.
- Delivery of US28 by incoming HCMV particles rapidly attenuates Akt activity to suppress HCMV lytic replication in monocytes.Science signaling · 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
- Potentially functional variants ofFrontiers in immunology · 2024Article
- Inhibition of SIRT2 promotes death of human cytomegalovirus-infected peripheral blood monocytes via apoptosis and necroptosis.Antiviral research · 2023Article
- Tyrosine Kinase Inhibitors Diminish Renal Neoplasms in a Tuberous Sclerosis Model Via Induction of Apoptosis.Molecular cancer therapeutics · 2023Article
- SLAMF7 regulates the inflammatory response in macrophages during polymicrobial sepsis.The Journal of clinical investigation · 2023Article
- Immunosuppressive Signaling Pathways as Targeted Cancer Therapies.Biomedicines · 2022Review
- Molecular interactions of adaptor protein PSTPIP2 control neutrophil-mediated responses leading to autoinflammation.Frontiers in immunology · 2022Article
- Inhibition of lipid phosphatase SHIP1 expands myeloid-derived suppressor cells and attenuates rheumatoid arthritis in mice.American journal of physiology. Cell physiology · 2021Article
- Article
- Genetic Approaches Using Zebrafish to Study the Microbiota-Gut-Brain Axis in Neurological Disorders.Cells · 2021Review
- Targeting SHIP1 and SHIP2 in Cancer.Cancers · 2021Review
- Interleukin-10 and Small Molecule SHIP1 Allosteric Regulators Trigger Anti-inflammatory Effects through SHIP1/STAT3 Complexes.iScience · 2020Article
- Human Cytomegalovirus Glycoprotein-Initiated Signaling Mediates the Aberrant Activation of Akt.Journal of virology · 2020Article
- Human Cytomegalovirus Mediates Unique Monocyte-to-Macrophage Differentiation through the PI3K/SHIP1/Akt Signaling Network.Viruses · 2020Article
- Excitable networks controlling cell migration during development and disease.Seminars in cell & developmental biology · 2020Review
- Lipid phosphatase SHIP-1 regulates chondrocyte hypertrophy and skeletal development.Journal of cellular physiology · 2020Article
- Article
- PI(3,4)P2 Signaling in Cancer and Metabolism.Frontiers in oncology · 2020Review
- Human Cytomegalovirus Induces an Atypical Activation of Akt To Stimulate the Survival of Short-Lived Monocytes.Journal of virology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The SH-2 containing inositol 5'-polyphosphatase 1 (SHIP1) is a multifunctional protein expressed predominantly, but not exclusively, by hematopoietic cells. SHIP1 removes the 5'-phosphate from the product of PI3K, PI(3,4,5)P₃, to generate PI(3,4)P₂. Both PIP species influence the activity level of Akt and ultimately regulate cell survival and differentiation. SHIP1 also harbors several protein interaction domains that endow it with many nonenzymatic cell signaling or receptor masking functions. In this review, we discuss the opposing roles of SHIP1 in cancer and in mucosal inflammation. On one hand, germline loss of SHIP1 causes myeloid lung consolidation and severe inflammation in the ileum, a phenotype that closely mimics human Crohn's disease and can be rescued by reconstitution with SHIP1-competent T cells. On the other, transient inhibition of the enzymatic activity of SHIP1 in cancer cells leads to apoptosis and enhances survival in lethal murine xenograft models. Overall, careful dissection of the different pathological mechanisms involved in several diseases provides novel opportunities for therapeutic intervention targeting SHIP1.
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.