ArticleBlood2010
Lyn- and PLC-beta3-dependent regulation of SHP-1 phosphorylation controls Stat5 activity and myelomonocytic leukemia-like disease.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Basal phosphorylation of SHIP1 by Lyn suppresses proinflammatory signaling in the absence of a phagocytic synapse.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Immunometabolic switch in hypertension: how dendritic cell mineralocorticoid receptors drive Th17 polarization and blood pressure control.European heart journal · 2025Article
- Neutrophil extracellular traps promote pre-metastatic niche formation in the omentum by expanding innate-like B cells that express IL-10.Cancer cell · 2025Article
- TREM2 aggravates sepsis by inhibiting fatty acid oxidation via the SHP1/BTK axis.The Journal of clinical investigation · 2024Article
- SHP-1 inhibition targets leukaemia stem cells to restore immunosurveillance and enhance chemosensitivity by metabolic reprogramming.Nature cell biology · 2024Article
- Induction of DNMT1-dependent demethylation of SHP-1 by the natural flavonoid compound Baicalein overcame Imatinib-resistance in CML CD34Cell communication and signaling : CCS · 2023Article
- Loss of Shp1 impairs myeloid cell function and causes lethal inflammation in zebrafish larvae.Disease models & mechanisms · 2023Article
- The roles of phospholipase C-β related signals in the proliferation, metastasis and angiogenesis of malignant tumors, and the corresponding protective measures.Frontiers in oncology · 2023Review
- Vitamin E Enhances Cancer Immunotherapy by Reinvigorating Dendritic Cells via Targeting Checkpoint SHP1.Cancer discovery · 2022Article
- Glycerophosphoinositol Promotes Apoptosis of Chronic Lymphocytic Leukemia Cells by Enhancing Bax Expression and Activation.Frontiers in oncology · 2022Article
- A targetable LIFR-NF-κB-LCN2 axis controls liver tumorigenesis and vulnerability to ferroptosis.Nature communications · 2021Article
- Runx proteins mediate protective immunity against Leishmania donovani infection by promoting CD40 expression on dendritic cells.PLoS pathogens · 2020Article
- Article
- STAT5: a Target of Antagonism by Neurotropic Flaviviruses.Journal of virology · 2019Article
- STAT3 and STAT5 Activation in Solid Cancers.Cancers · 2019Review
- Article
- SHP-1 regulates hematopoietic stem cell quiescence by coordinating TGF-β signaling.The Journal of experimental medicine · 2018Article
- Positive and Negative Regulatory Roles of C-Terminal Src Kinase (CSK) in FcεRI-Mediated Mast Cell Activation, Independent of the Transmembrane Adaptor PAG/CSK-Binding Protein.Frontiers in immunology · 2018Article
- PDZK1 inhibits the development and progression of renal cell carcinoma by suppression of SHP-1 phosphorylation.Oncogene · 2017Article
- M. tuberculosis-Initiated Human Mannose Receptor Signaling Regulates Macrophage Recognition and Vesicle Trafficking by FcRγ-Chain, Grb2, and SHP-1.Cell reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperactivation of the transcription factor Stat5 leads to various leukemias. Stat5 activity is regulated by the protein phosphatase SHP-1 in a phospholipase C (PLC)-β3-dependent manner. Thus, PLC-β3-deficient mice develop myeloproliferative neoplasm, like Lyn (Src family kinase)- deficient mice. Here we show that Lyn/PLC-β3 doubly deficient lyn(-/-);PLC-β3(-/-) mice develop a Stat5-dependent, fatal myelodysplastic/myeloproliferative neoplasm, similar to human chronic myelomonocytic leukemia (CMML). In hematopoietic stem cells of lyn(-/-);PLC-β3(-/-) mice that cause the CMML-like disease, phosphorylation of SHP-1 at Tyr(536) and Tyr(564) is abrogated, resulting in reduced phosphatase activity and constitutive activation of Stat5. Furthermore, SHP-1 phosphorylation at Tyr(564) by Lyn is indispensable for maximal phosphatase activity and for suppression of the CMML-like disease in these mice. On the other hand, Tyr(536) in SHP-1 can be phosphorylated by Lyn and another kinase(s) and is necessary for efficient interaction with Stat5. Therefore, we identify a novel Lyn/PLC-β3-mediated regulatory mechanism of SHP-1 and Stat5 activities.
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