ArticleMolecular and cellular biology2000
Both src-dependent and -independent mechanisms mediate phosphatidylinositol 3-kinase regulation of colony-stimulating factor 1-activated mitogen-activated protein kinases in myeloid progenitors.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 100 citations in OpenAlex.
- Phase II study of dasatinib in patients with previously treated malignant mesothelioma (cancer and leukemia group B 30601): a brief report.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2012Trial
- Unveiling the Involvement of Extracellular Vesicles in Breast Cancer's Organotrophic Metastasis: Molecular Mechanisms and Translational Prospects.International journal of molecular sciences · 2025Review
- Pharmacological impacts of tanshinone on osteogenesis and osteoclastogenesis: a review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Review
- Phospholipase D2 controls bone homeostasis by modulating M-CSF-dependent osteoclastic cell migration and microtubule stability.Experimental & molecular medicine · 2022Article
- Potential Stereoselective Binding ofMolecules (Basel, Switzerland) · 2022Article
- Construction and validation of a novel and superior protein risk model for prognosis prediction in esophageal cancer.Frontiers in genetics · 2022Article
- Article
- Two macrophages, osteoclasts and microglia: from development to pleiotropy.Bone research · 2021Review
- ELMO1 Regulates RANKL-Stimulated Differentiation and Bone Resorption of Osteoclasts.Frontiers in cell and developmental biology · 2021Article
- Grape Seed Proanthocyanidin Extract Prevents Bone Loss via Regulation of Osteoclast Differentiation, Apoptosis, and Proliferation.Nutrients · 2020Article
- Review
- A Synthetic Peptide, CK2.3, Inhibits RANKL-Induced Osteoclastogenesis through BMPRIa and ERK Signaling Pathway.Journal of developmental biology · 2020Article
- Molecular mechanisms and clinical management of cancer bone metastasis.Bone research · 2020Review
- Small molecule immunomodulation: the tumor microenvironment and overcoming immune escape.Journal for immunotherapy of cancer · 2019Review
- Molecular signaling in bone cells: Regulation of cell differentiation and survival.Advances in protein chemistry and structural biology · 2019Review
- A ERK/RSK-mediated negative feedback loop regulates M-CSF-evoked PI3K/AKT activation in macrophages.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Article
- Signaling Pathways in Osteoclast Differentiation.Chonnam medical journal · 2016Review
- SHP2 regulates osteoclastogenesis by promoting preosteoclast fusion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Colony-stimulating factor 1 (CSF-1) supports the proliferation, survival, and differentiation of bone marrow-derived cells of the monocytic lineage. In the myeloid progenitor 32D cell line expressing CSF-1 receptor (CSF-1R), CSF-1 activation of the extracellular signal-regulated kinase (ERK) pathway is both Ras and phosphatidylinositol 3-kinase (PI3-kinase) dependent. PI3-kinase inhibition did not influence events leading to Ras activation. Using the activity of the PI3-kinase effector, Akt, as readout, studies with dominant-negative and oncogenic Ras failed to place PI3-kinase downstream of Ras. Thus, PI3-kinase appears to act in parallel to Ras. PI3-kinase inhibitors enhanced CSF-1-stimulated A-Raf and c-Raf-1 activities, and dominant-negative A-Raf but not dominant-negative c-Raf-1 reduced CSF-1-provoked ERK activation, suggesting that A-Raf mediates a part of the stimulatory signal from Ras to MEK/ERK, acting in parallel to PI3-kinase. Unexpectedly, a CSF-1R lacking the PI3-kinase binding site (DeltaKI) remained capable of activating MEK/ERK in a PI3-kinase-dependent manner. To determine if Src family kinases (SFKs) are involved, we demonstrated that CSF-1 activated Fyn and Lyn in cells expressing wild-type (WT) or DeltaKI receptors. Moreover, CSF-1-induced Akt activity in cells expressing DeltaKI is SFK dependent since Akt activation was prevented by pharmacological or genetic inhibition of SFK activity. The docking protein Gab2 may link SFK to PI3-kinase. CSF-1 induced Gab2 tyrosyl phosphorylation and association with PI3-kinase in cells expressing WT or DeltaKI receptors. However, only in DeltaKI cells are these events prevented by PP1. Thus in myeloid progenitors, CSF-1 can activate the PI3-kinase/Akt pathway by at least two mechanisms, one involving direct receptor binding and one involving SFKs.
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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.