ArticleBlood2013
Megakaryocyte-specific deletion of the protein-tyrosine phosphatases Shp1 and Shp2 causes abnormal megakaryocyte development, platelet production, and function.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 110 citations in OpenAlex.
- MPIG6B-related thrombocytopenia and myelofibrosis: A case report.Annals of hematology · 2026Article
- Platelet Membrane Receptors and Signalling Pathways.Handbook of experimental pharmacology · 2026Review
- Synergistic effects of deleting the tyrosine phosphatases Shp1 and Shp2 on megakaryopoiesis and thrombopoiesis in mice.bioRxiv : the preprint server for biology · 2025Article
- Platelets and diseases: signal transduction and advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Angiopoietin-like protein 2 inhibits thrombus formation.Molecular and cellular biochemistry · 2025Article
- The involvement of krüppel-like transcription factor 2 in megakaryocytic differentiation induction by phorbol 12-myrestrat 13-acetate.Biomarker research · 2024Article
- Loss of neutrophil Shp1 produces hemorrhagic and lethal acute lung injury.bioRxiv : the preprint server for biology · 2024Article
- Platelet RNA sequencing reveals profile of caffeic acid affecting hemostasis in mice.Research and practice in thrombosis and haemostasis · 2024Article
- ABIN1 (Q478) is Required to Prevent Hematopoietic Deficiencies through Regulating Type I IFNs Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Comprehensive analysis of serum exosome-derived lncRNAs and mRNAs from patients with rheumatoid arthritis.Arthritis research & therapy · 2023Article
- Regulation of Glycoprotein VI-Dependent Platelet Activation and Thrombus Formation by Heparan Sulfate Proteoglycan Perlecan.International journal of molecular sciences · 2023Article
- Article
- Treatment of congenital thrombocytopenia and decreased collagen reactivity in G6b-B-deficient mice.Blood advances · 2023Article
- Experimental validation of computerised models of clustering of platelet glycoprotein receptors that signal via tandem SH2 domain proteins.PLoS computational biology · 2022Article
- G6b-B regulates an essential step in megakaryocyte maturation.Blood advances · 2022Article
- RASopathies and hemostatic abnormalities: key role of platelet dysfunction.Orphanet journal of rare diseases · 2021Article
- A New Paradigm for KIM-PTP Drug Discovery: Identification of Allosteric Sites with Potential for Selective Inhibition Using Virtual Screening and LEI Analysis.International journal of molecular sciences · 2021Article
- Differences in the Platelet mRNA Landscape Portend Racial Disparities in Platelet Function and Suggest Novel Therapeutic Targets.Clinical pharmacology and therapeutics · 2021Article
- Prolonged thrombocytopenia in a neonate with Noonan syndrome: a case report.The Journal of international medical research · 2020Article
- Control of Innate Immunity by Sialic Acids in the Nervous Tissue.International journal of molecular sciences · 2020Review
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7 authors at 3 institutions in 2 countries.
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Abstract
The SH2 domain-containing protein-tyrosine phosphatases Shp1 and Shp2 have been implicated in regulating signaling from a variety of platelet and megakaryocyte receptors. In this study, we investigate the functions of Shp1 and Shp2 in megakaryocytes and platelets. Megakaryocyte/platelet (MP)-specific deletion of Shp1 in mice resulted in platelets being less responsive to collagen-related peptide due to reduced GPVI expression and signaling via the Src family kinase (SFK)-Syk-PLCγ2 pathway, and fibrinogen due to reduced SFK activity. By contrast, deletion of Shp2 in the MP lineage resulted in macrothrombocytopenia and platelets being hyper-responsive to anti-CLEC-2 antibody and fibrinogen. Shp1- and Shp2-deficient megakaryocytes had partial blocks at 2N/4N ploidy; however, only the latter exhibited reduced proplatelet formation, thrombopoietin, and integrin signaling. Mice deficient in both Shp1 and Shp2 were severely macrothrombocytopenic and had reduced platelet surface glycoprotein expression, including GPVI, αIIbβ3, and GPIbα. Megakaryocytes from these mice were blocked at 2N/4N ploidy and did not survive ex vivo. Deletion of the immunoreceptor tyrosine-based inhibition motif-containing receptor G6b-B in the MP lineage phenocopied multiple features of Shp1/2-deficient mice, suggesting G6b-B is a critical regulator of Shp1 and Shp2. This study establishes Shp1 and Shp2 as major regulators of megakaryocyte development, platelet production, and function.
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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.