ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Cross-Talk between Shp1 and PIPKIγ Controls Leukocyte Recruitment.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Biallelic loss-of-function PTPN6 variants lead to inflammatory lung disease and hemolytic anemia.The Journal of experimental medicine · 2026Article
- The Endothelial Glycocalyx as a Target of Excess Soluble Fms-like Tyrosine Kinase-1.International journal of molecular sciences · 2023Article
- Loss of Shp1 impairs myeloid cell function and causes lethal inflammation in zebrafish larvae.Disease models & mechanisms · 2023Article
- Selectin-Mediated Signaling-Shedding Light on the Regulation of Integrin Activity in Neutrophils.Cells · 2022Review
- Systemic Inflammatory Markers of Resectable Colorectal Cancer Patients with Different Mismatch Repair Gene Status.Cancer management and research · 2021Article
- Modeling of the immune response in the pathogenesis of solid tumors and its prognostic significance.Cellular oncology (Dordrecht, Netherlands) · 2020Review
- Type Iγ phosphatidylinositol phosphate kinase promotes tumor growth by facilitating Warburg effect in colorectal cancer.EBioMedicine · 2019Article
- PIPKIJournal of immunology research · 2019Article
- SHP-1 regulates hematopoietic stem cell quiescence by coordinating TGF-β signaling.The Journal of experimental medicine · 2018Article
- Suppression of PTPN6 exacerbates aluminum oxide nanoparticle-induced COPD-like lesions in mice through activation of STAT pathway.Particle and fibre toxicology · 2017Article
- Shp1 function in myeloid cells.Journal of leukocyte biology · 2017Review
- Repurposing Treatments to Enhance Innate Immunity. Can Statins Improve Neutrophil Functions and Clinical Outcomes in COPD?Journal of clinical medicine · 2016Review
- Protein tyrosine phosphatase SHP-1: resurgence as new drug target for human autoimmune disorders.Immunologic research · 2016Review
- Immunoreceptors on neutrophils.Seminars in immunology · 2016Review
- Discovery and replication of a peripheral tissue DNA methylation biosignature to augment a suicide prediction model.Clinical epigenetics · 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
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Neutrophil recruitment to the site of inflammation plays a pivotal role in host defense. However, overwhelming activation and accumulation of neutrophils in the tissue may cause tissue damage and autoimmunity due to the release of cytokines, oxidants, and proteases. Neutrophil adhesion in acute inflammation is initiated by activation of αLβ2 (LFA-1), which can be induced by rolling on E-selectin (slowly) or by exposure to the chemokine CXCL1 (rapidly). Despite the clinical importance, cell-intrinsic molecular mechanisms of negative regulation of integrin adhesiveness and neutrophil recruitment are poorly understood. Mice deficient in the tyrosine phosphatase Src homology 2 domain-containing protein tyrosine phosphatase 1 (Shp1) show increased leukocyte adhesion, but the interpretation of these data is limited by the severe global phenotype of these mice. In this study, we used mice with global and myeloid-restricted deletion of Shp1 to study neutrophil arrest, adhesion, crawling, and transendothelial migration in vitro and in vivo. Shp1 deficiency results in increased neutrophil adhesion in vivo; however, neutrophil crawling, transmigration, and chemotaxis were reduced in these mice. Mechanistically, Shp1 binds and controls PIPKIγ activity and, thereby, modulates phosphatidylinositol (4,5)-bisphosphate levels and adhesion. Thus, Shp1 is involved in the deactivation of integrins and regulation of neutrophil recruitment into inflamed tissue.
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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.