ArticleBlood2005
p85alpha subunit of class IA PI-3 kinase is crucial for macrophage growth and migration.
Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 66 citations in OpenAlex.
- Phosphoinositide Signaling in Immune Cell Migration.Biomolecules · 2023Review
- Colony-stimulating factor 1 receptor signaling in the central nervous system and the potential of its pharmacological inhibitors to halt the progression of neurological disorders.Inflammopharmacology · 2022Review
- M2 macrophages, but not M1 macrophages, support megakaryopoiesis by upregulating PI3K-AKT pathway activity.Signal transduction and targeted therapy · 2021Article
- Class IA PI3K regulatory subunits: p110-independent roles and structures.Biochemical Society transactions · 2020Review
- Colony-Stimulating Factor 1 Receptor (CSF1R) Activates AKT/mTOR Signaling and Promotes T-Cell Lymphoma Viability.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- PI3K p85α Subunit-deficient Macrophages Protect Mice from Acute Colitis due to the Enhancement of IL-10 Production.Scientific reports · 2017Article
- Cytokine mediators of chronic graft-versus-host disease.The Journal of clinical investigation · 2017Review
- Metabolic Reprogramming Mediated by the mTORC2-IRF4 Signaling Axis Is Essential for Macrophage Alternative Activation.Immunity · 2016Article
- ROCK1 via LIM kinase regulates growth, maturation and actin based functions in mast cells.Oncotarget · 2016Article
- Macrophage motility is driven by frontal-towing with a force magnitude dependent on substrate stiffness.Integrative biology : quantitative biosciences from nano to macro · 2015Article
- Two-dimensional motility of a macrophage cell line on microcontact-printed fibronectin.Cytoskeleton (Hoboken, N.J.) · 2014Article
- Innate immune regulation by STAT-mediated transcriptional mechanisms.Immunological reviews · 2014Review
- CSF-1 receptor signaling in myeloid cells.Cold Spring Harbor perspectives in biology · 2014Review
- Generation of membrane structures during phagocytosis and chemotaxis of macrophages: role and regulation of the actin cytoskeleton.Immunological reviews · 2013Review
- rna interference targeting p110β reduces tumor necrosis factor-alpha production in cellular response to wear particles in vitro and osteolysis in vivo.Inflammation · 2013Article
- Phosphoinositides: tiny lipids with giant impact on cell regulation.Physiological reviews · 2013Review
- Alveolar epithelial cells are critical in protection of the respiratory tract by secretion of factors able to modulate the activity of pulmonary macrophages and directly control bacterial growth.Infection and immunity · 2013Article
- Impaired function of Fanconi anemia type C-deficient macrophages.Journal of leukocyte biology · 2012Article
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Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Macrophages play an essential role in defending against invading pathogens by migrating to the sites of infection, removing apoptotic cells, and secreting inflammatory cytokines. The molecular mechanisms whereby macrophages regulate these processes are poorly understood. Using bone marrow-derived macrophages (BMMs) deficient in the expression of p85alpha-subunit of class IA phosphatidylinositol 3 (PI-3) kinase, we demonstrate 50% reduction in proliferation in response to macrophage-colony-stimulating factor (M-CSF) as well as granulocyte macrophage-colony-stimulating factor (GM-CSF) compared with wild-type controls. Furthermore, p85alpha-/- BMMs demonstrate a significant reduction in migration in a wound-healing assay compared with wild-type controls. The reduction in migration due to p85alpha deficiency in BMMs is associated with reduced adhesion and directed migration on fibronectin and vascular cell adhesion molecule-1. In addition, deficiency of p85alpha in BMMs also results in defective phagocytosis of sheep red blood cells. Biochemically, loss of p85alpha in BMMs results in reduced activation of Akt and Rac, but not Erk (extracellular signal-related kinase) mitogen-activated protein (MAP) kinase. Taken together, our results provide genetic evidence for the importance of p85alpha in regulating both actin- and growth-based functions in macrophages, and provide a potential therapeutic target for the treatment of diseases involving macrophages, including inflammation.
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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.