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rdf:type |
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lifeskim:mentions |
umls-concept:C0079459,
umls-concept:C0332281,
umls-concept:C0334094,
umls-concept:C0439831,
umls-concept:C0752312,
umls-concept:C0871261,
umls-concept:C1704259,
umls-concept:C1704632,
umls-concept:C1705987,
umls-concept:C1706817,
umls-concept:C1710082,
umls-concept:C1879547,
umls-concept:C2911692
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pubmed:issue |
4
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pubmed:dateCreated |
1994-3-29
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pubmed:abstractText |
Granulocyte colony-stimulating factor (G-CSF) can elicit responses that include proliferation, granulocytic differentiation, and activation of cellular functions in target cells. The biochemical pathways responsible for transduction of these signals from the G-CSF receptor (G-CSFR) have not been defined. In this report, we show that, in murine (NFS-60) and human (OCI-AML 1) myeloid leukemia cell lines and in murine pro-B-lymphocytic cells, BAF/B03, transfected with the murine G-CSFR, proliferative responses to G-CSF are associated with rapid activation of p42 and p44 MAP kinases and p21ras. Truncation of the cytoplasmic portion of the murine G-CSFR at residue 646 but not at residue 739 abolished G-CSF-induced stimulation of cellular proliferation as well as activation of MAP kinase and p21ras in transfected BAF/B03 cells. G-CSF-induced granulocytic differentiation of the murine leukemic cell line 32DC13(G) occurred in the absence of detectable activation of p42 MAP kinase. Nonproliferative responses to G-CSF in the human promyelocytic cell line HL-60 and in human neutrophils were similarly associated with no MAP kinase activation. These results imply that differing cellular effects of G-CSF may be involve the recruitment of differing signal transduction pathways with the p21ras/MAP kinase pathway being limited to proliferative responses.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0006-4971
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
83
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
949-57
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:7509213-Animals,
pubmed-meshheading:7509213-B-Lymphocytes,
pubmed-meshheading:7509213-Calcium-Calmodulin-Dependent Protein Kinases,
pubmed-meshheading:7509213-Cell Differentiation,
pubmed-meshheading:7509213-Cell Division,
pubmed-meshheading:7509213-Cell Line,
pubmed-meshheading:7509213-Enzyme Activation,
pubmed-meshheading:7509213-Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:7509213-Guanosine Triphosphate,
pubmed-meshheading:7509213-Humans,
pubmed-meshheading:7509213-Interleukin-3,
pubmed-meshheading:7509213-Kinetics,
pubmed-meshheading:7509213-Leukemia, Myeloid,
pubmed-meshheading:7509213-Leukemia, Promyelocytic, Acute,
pubmed-meshheading:7509213-Mice,
pubmed-meshheading:7509213-Proto-Oncogene Proteins p21(ras),
pubmed-meshheading:7509213-Receptors, Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:7509213-Recombinant Proteins,
pubmed-meshheading:7509213-Signal Transduction,
pubmed-meshheading:7509213-Transfection,
pubmed-meshheading:7509213-Tumor Cells, Cultured
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pubmed:year |
1994
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pubmed:articleTitle |
Proliferative but not nonproliferative responses to granulocyte colony-stimulating factor are associated with rapid activation of the p21ras/MAP kinase signalling pathway.
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pubmed:affiliation |
Section of Cell and Molecular Biology, Chester Beatty Laboratories, Institute of Cancer Research, London, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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