Colony-stimulating factor (CSF) controls proliferation of CSF-dependent cells by acting during the G1 phase of the cell cycle.

Pluznik, Dov H.; Cunningham, Robert E.; Noguchi, Philip D.

doi:10.1073/pnas.81.23.7451

Cited by 31 publications

(15 citation statements)

References 19 publications

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“…As shown in Fig. 3, accumulation of GTP-bound active p21 could be observed after the addition of IL-3 in all three IL-3-dependent cell lines: pre-B-cell line BAF3 (14) and mast cell lines IC2 (15) and PT18 (16). The fold increase ofthe ratio of p21-GTP to total p21 was +:: : : : : :: : : : : : .…”

Section: Resultsmentioning

confidence: 78%

Involvement of ras p21 protein in signal-transduction pathways from interleukin 2, interleukin 3, and granulocyte/macrophage colony-stimulating factor, but not from interleukin 4.

Satoh

Nakafuku

Miyajima

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

318

148

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The protooncogene ras acts as a component of signal-transduction networks in many kinds of cells. The ras gene product (p21) is a GTP-binding protein, and the activity of the protein is regulated by bound GDP/GTP. Recent studies have shown that a certain class of growth factors stimulates the formation of active p2lFGTP complexes in fibroblasts and that oncogene products with enhanced tyrosine kinase activities have a similar effect on ras p21. We have measured the ratio of active GTP-bound p21 to total p21 in several lymphoid and myeloid cell lines in order to understand the role of ras in the proliferation of these cells. Interleukin 2 (IL-2), IL-3, and granulocyte/macrophage colony-stimulating factor (GM-CSF) enhance the formation of the active p21GTP, whereas IL4 has no effect on p21-bound GDP/GTP. These results strongly suggest that ras p21 acts as a transducer of signals from IL-2, IL-3, and GM-CSF, but not from IL-4.

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Section: Resultsmentioning

confidence: 78%

Involvement of ras p21 protein in signal-transduction pathways from interleukin 2, interleukin 3, and granulocyte/macrophage colony-stimulating factor, but not from interleukin 4.

Satoh

Nakafuku

Miyajima

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

318

148

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“…Interestingly, the early G1 phase is also an important phase in the cell cycle for cells depending on CSF for their proliferation (11). The presence of GM-CSF in early G1 is essential to enable PT-18 cells to continue to progress through the cell cycle.…”

Section: Resultsmentioning

confidence: 99%

“…MLCM was prepared according to Burgess et al (10) with slight modifications as described (11). It is known that MLCM contains two subclasses of CSF (GM-CSF and G-CSF; ref.…”

Section: Methodsmentioning

confidence: 99%

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Colony stimulating factor-induced differentiation of murine M1 myeloid leukemia cells is permissive in early G1 phase.

Tsuda¹,

Neckers²,

Pluznik³

1986

Proc. Natl. Acad. Sci. U.S.A.

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Granulocyte-colony stimulating factor (G-CSF) induces differentiation of M1 murine myeloid leukemia cells into mature granulocytes/macrophages and also causes accumulation of the cells in the G1 phase of the cell cycle. We examined, therefore, whether synchronization of M1 cells in the G1 phase could affect G-CSF-induced differentiation as quantitated by expression of Fc fragment receptors (FcR) and lysozyme activity. Cells were arrested in early G1 by density inhibition in the absence of serum and in late G1 by addition of aphidicolin. Cells synchronized in early G1, when stimulated with G-CSF, showed enhanced expression of FcR and lysozyme activity. Eighty percent of the cells expressed FcR 18 hr after addition of G-CSF while, in exponentially growing cells, this percentage was reached 72 hr after addition of G-CSF. Cells synchronized in late G1 did not show enhanced expression of differentiation markers. These results imply that with respect to G-CSF-induced differentiation, the G1 phase can be separated into an early permissive and a later nonpermissive stage.

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“…However, recent experiments have demonstrated that macrophage giant cells do regulate the replication and differentiation of myeloid (macrophage-granulocyte) progenitor cells (18)(19)(20) are well defined and have been termed colony-stimulating factors (CSFs).' Four CSFs have been described: interleukin 3 (IL-3 or multi-CSF), granulocyte-macrophage colony stimulating factor (GM-CSF), colony-stimulating factor 1 (CSF-1, or M-CSF) and granulocyte colony-stimulating factor (G-CSF).…”

Section: Introductionmentioning

confidence: 99%

Colony-stimulating factors regulate the development of multinucleated osteoclasts from recently replicated cells in vitro.

Lorenzo¹,

Sousa²,

Fonseca³

et al. 1987

J. Clin. Invest.

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Osteoclasts mediate the process of bone resorption. However These results demonstrate that GM-CSF and IL-3 can regulate the development of osteoclasts from recently replicated precursor cells in cultured fetal mouse long bones. However, the mechanisms by which CSFs influence osteoclast formation are difficult to determine from these studies because markers for the osteoclast progenitor and precursor do not exist. These data also provide evidence that the differentiation of osteoclast progenitors is regulated by different factors at different points in their ontogeny.

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Colony-stimulating factor (CSF) controls proliferation of CSF-dependent cells by acting during the G1 phase of the cell cycle.

Cited by 31 publications

References 19 publications

Involvement of ras p21 protein in signal-transduction pathways from interleukin 2, interleukin 3, and granulocyte/macrophage colony-stimulating factor, but not from interleukin 4.

Involvement of ras p21 protein in signal-transduction pathways from interleukin 2, interleukin 3, and granulocyte/macrophage colony-stimulating factor, but not from interleukin 4.

Colony stimulating factor-induced differentiation of murine M1 myeloid leukemia cells is permissive in early G1 phase.

Colony-stimulating factors regulate the development of multinucleated osteoclasts from recently replicated cells in vitro.

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