ArticleProceedings of the National Academy of Sciences of the United States of America1994
Granulocyte colony-stimulating factor receptor signaling involves the formation of a three-component complex with Lyn and Syk protein-tyrosine kinases.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 213 citations in OpenAlex.
- Colony-Stimulating Factor 3 Receptor Mutations and Variants in Hematological Malignancies.Cancers · 2025Review
- The dualistic role of Lyn tyrosine kinase in immune cell signaling: implications for systemic lupus erythematosus.Frontiers in immunology · 2024Review
- Review
- DRUGGING "UNDRUGGABLE" DISEASE-CAUSING PROTEINS: FOCUS ON SIGNAL TRANSDUCER AND ACTIVATOR OF TRANSCRIPTION (STAT) 3.Transactions of the American Clinical and Climatological Association · 2022Article
- A review of granulocyte colony-stimulating factor receptor signaling and regulation with implications for cancer.Frontiers in oncology · 2022Review
- The Src-family Kinase Lyn in Immunoreceptor Signaling.Endocrinology · 2021Review
- Current Management of Chronic Neutrophilic Leukemia.Current treatment options in oncology · 2021Review
- Neuroprotection through G-CSF: recent advances and future viewpoints.Pharmacological reports : PR · 2021Review
- Targeting few to help hundreds: JAK, MAPK and ROCK pathways as druggable targets in atypical chronic myeloid leukemia.Molecular cancer · 2018Review
- Chronic neutrophilic leukemia: new science and new diagnostic criteria.Blood cancer journal · 2018Review
- Article
- Granulocyte colony-stimulating factor receptor signaling in severe congenital neutropenia, chronic neutrophilic leukemia, and related malignancies.Experimental hematology · 2017Review
- Granulocyte Colony-Stimulating Factor and Its Potential Application for Skeletal Muscle Repair and Regeneration.Mediators of inflammation · 2017Review
- Article
- Molecular pathogenesis of atypical CML, CMML and MDS/MPN-unclassifiable.International journal of hematology · 2015Review
- CSF3R, SETBP1 and CALR mutations in chronic neutrophilic leukemia.Journal of hematology & oncology · 2014Article
- Ligand independence of the T618I mutation in the colony-stimulating factor 3 receptor (CSF3R) protein results from loss of O-linked glycosylation and increased receptor dimerization.The Journal of biological chemistry · 2014Article
- Systems approach to phagocyte production and activation: neutrophils and monocytes.Advances in experimental medicine and biology · 2014Review
- Granulocyte colony-stimulating factor receptor mutations in myeloid malignancy.Frontiers in oncology · 2014Review
- Neutrophil cell surface receptors and their intracellular signal transduction pathways.International immunopharmacology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein that critically regulates the viability, proliferation, and differentiation of granulocytic precursors and the function of neutrophils by signaling through its receptor. Cloning of the human G-CSF receptor (G-CSFR) cDNA has demonstrated sequence homology with other members of the hematopoietic/cytokine receptor superfamily. G-CSF stimulates the appearance of phosphotyrosine proteins in several types of human and murine myeloid cells. Since the receptor does not possess intrinsic tyrosine kinase activity, we hypothesized that G-CSFR interacts with and activates cytosolic protein-tyrosine kinases (PTKs). In vitro protein kinase assay of human G-CSFR immunoprecipitates demonstrated at least two tyrosine phosphoproteins, pp55 and pp70. We observed that G-CSF activated p53/p56lyn, a Src-related PTK, and p72syk, a non-Src-related PTK. Lyn and Syk were recovered in anti-G-CSFR immunoprecipitates; Lyn was detected in the absence of ligand. In addition, upon G-CSF stimulation, Lyn coimmunoprecipitated with Syk. Analysis of the G-CSFR amino acid sequence revealed a potential receptor activation motif for Syk. On the basis of immunoprecipitation and sequence analysis data, we propose that the human G-CSFR forms a three-component signaling complex with Lyn and Syk. Their sequential recruitment into the G-CSFR signaling complex demonstrates the coordinated involvement of two PTKs with a member of the hematopoietic/cytokine receptor superfamily.
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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.