Control of mammalian cell proliferation

Zetterberg, Anders

doi:10.1016/0955-0674(90)90022-7

Cited by 25 publications

(8 citation statements)

References 18 publications

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“…The cell transition from the quiescent to the proliferative state (GO->GI) requires an increase in the rate of RNA and protein synthesis (GI phase) necessary for cells to replicate their DNA (S phase) (64)(65)(66)(67)(68)(69)(70). We analyzed the effect of bFGF (1 and 25 ng/ml) on RNA, protein and DNA synthesis by using synchronized HUVE cells prior to or after exposure of the cells to TCM (Fig.…”

Section: Methodsmentioning

confidence: 99%

Cytokines from activated T cells induce normal endothelial cells to acquire the phenotypic and functional features of AIDS-Kaposi's sarcoma spindle cells.

Fiorelli¹,

Gendelman²,

Samaniego³

et al. 1995

J. Clin. Invest.

148

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Kaposi's sarcoma (KS) is a proliferative disease of vascular origin particularly frequent in HIV-1-infected homosexual men (AIDS-KS) and characterized by proliferating spindleshaped cells, angiogenesis, and inflammatory cell infiltration. Previous work has suggested that KS spindle cells are of endothelial cell origin and that chronic immune activation via the release of inflammatory cytokines may cooperate with basic fibroblast growth factor (bFGF) and the HIV-1 Tat protein in the induction and progression of AIDS-KS. Invest. 1995Invest. .95:1723Invest. -1734

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Section: Methodsmentioning

confidence: 99%

Cytokines from activated T cells induce normal endothelial cells to acquire the phenotypic and functional features of AIDS-Kaposi's sarcoma spindle cells.

Fiorelli¹,

Gendelman²,

Samaniego³

et al. 1995

J. Clin. Invest.

148

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“…In addition to nutrients mammalian cells require extracellular growth factors to grow and proliferate (Conlon and Raff, 1999; Pardee, 1989; Sherr, 1994; Zetterberg, 1990). Absent such factors, many types of cells survive in a quiescent or G0 state.…”

Section: Introductionmentioning

confidence: 99%

Proteomic and Metabolomic Characterization of a Mammalian Cellular Transition from Quiescence to Proliferation

et al. 2017

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SUMMARY There exist similarities and differences in metabolism and physiology between normal proliferative cells and tumor cells. Once a cell enters the cell cycle, metabolic machinery is engaged to facilitate various processes. The kinetics and regulation of these metabolic changes have not been properly evaluated. To correlate the orchestration of these processes with the cell cycle, we analyzed the transition from quiescence to proliferation of a non-malignant murine pro-B lymphocyte cell line in response to IL-3. Using multiplex mass-spectrometry-based proteomics we show that the transition to proliferation shares features generally attributed to cancer cells: up-regulation of glycolysis, lipid metabolism, amino-acid synthesis, and nucleotide synthesis and down-regulation of oxidative phosphorylation and the urea cycle. Furthermore, metabolomic profiling of this transition reveals similarities to cancer-related metabolic pathways. In particular, we find that methionine is consumed at a higher rate than other essential amino acids, with a potential link to epigenetic maintenance.

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“…In Go-arrested cells, a similar inhibitor of Cdk2 kinase was detected. These data suggest the existence of an inhibitor of cyclin-dependent kinases induced under different conditions to mediate antiproliferative responses.Control of the eukaryotic cell cycle occurs at key points in G, and at the G2-to-M phase transition (41,80,85,121,122). These transitions are governed by multimeric protein complexes with serine/threonine kinase activity, whose catalytic subunits, proteins of 33 to 34 kDa, are regulated by phosphorylation and by periodic association with positive effector proteins, known as cyclins.…”

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confidence: 99%

“…Inhibition of protein synthesis or transfer to 1% serum in early G, prior to the restriction point prevents cell cycle progression and causes cells to enter into a quiescent state, Go. After passing the restriction point, a cell is committed to a replication cycle and nutrient deprivation fails to prevent the transition to S phase (84,121). Because of this apparent parallel between G, control in yeast and animal cells, it is of interest to determine whether mitogenic and growth-inhibitory signals in mammalian cells are mediated at the level of cyclins and cyclin-dependent kinases, as they are in yeast cells.…”

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confidence: 99%

A novel inhibitor of cyclin-Cdk activity detected in transforming growth factor beta-arrested epithelial cells.

Slingerland¹,

Hengst²,

Pan³

et al. 1994

Mol. Cell. Biol.

301

186

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Transforming growth factor , (TGF-,B) is a potent inhibitor of epithelial cell growth. Cyclins E and A in association with Cdk2 have been shown to play a role in the GI-to-S phase transition in mammalian cells. We have studied the effects of TGF-p-mediated growth arrest on GJ/S cyclins E and A. Inhibition of cyclin A-associated kinase by TGF-j is primarily due to a decrease in cyclin A mRNA and protein. By contrast, while TGF-0 inhibits accumulation of cyclin E mRNA, the reduction in cyclin E protein is minimal. Instead, we find that the activation of cyclin E-associated kinase that normally accompanies the Gl-to-S phase transition is inhibited. A novel inhibitor of cyclin-Cdk complexes was detected in TGF-j8-treated cell lysates. Inhibition is mediated by a heat-stable protein that targets both Cdk2 and Cdc2 kinases. In Go-arrested cells, a similar inhibitor of Cdk2 kinase was detected. These data suggest the existence of an inhibitor of cyclin-dependent kinases induced under different conditions to mediate antiproliferative responses.Control of the eukaryotic cell cycle occurs at key points in G, and at the G2-to-M phase transition (41,80,85,121,122). These transitions are governed by multimeric protein complexes with serine/threonine kinase activity, whose catalytic subunits, proteins of 33 to 34 kDa, are regulated by phosphorylation and by periodic association with positive effector proteins, known as cyclins. Current understanding of cell cycle control derives largely from studies of yeast cells. The Cdc28 kinase in the budding yeast Saccharomyces cerevisiae and its homolog in the fission yeast Schizosaccharomycespombe, Cdc2, appear to regulate both the Gl-to-S and G2-to-M phase transitions (5,81,88,93,95). In S. cerevisiae, association of p34Cdc28 with Gl cyclins, or Clns, is necessary for entry to S phase (12,38,77,98,115), while association with the mitotic or B-type cyclins, the Clbs, promotes entry into mitosis (30, 108).The first human homolog of p34Cdc2/Cdc28 to be identified, Cdc2Hs, could complement p34 deficiency in both S. cerevisiae and S. pombe (16, 61). However, its action appears to be restricted to the G2-to-M phase transition in humans (15,89,97,110).A number of Cdc2-related or cyclin-dependent kinases (Cdks) have subsequently been identified (23,51,61,74,78,86,102,112). These kinases combine with different cyclins to govern different cell cycle transitions. One of these, Cdk2, appears to regulate Gl-and S-phase functions in human cells (62,102,113). The action of Cdk2 in complex with cyclin A is essential for progression through S phase and may play a role in the regulation of DNA synthesis (25,32,33,83,90,123).Several candidate G, cyclins, designated C, D, and E, were identified when human and Drosophila cDNA libraries were screened for sequences that could complement deletion of the S. cerevisiae Cln genes (51,63,65,117). A cyclin D cDNA was

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Control of mammalian cell proliferation

Cited by 25 publications

References 18 publications

Cytokines from activated T cells induce normal endothelial cells to acquire the phenotypic and functional features of AIDS-Kaposi's sarcoma spindle cells.

Cytokines from activated T cells induce normal endothelial cells to acquire the phenotypic and functional features of AIDS-Kaposi's sarcoma spindle cells.

Proteomic and Metabolomic Characterization of a Mammalian Cellular Transition from Quiescence to Proliferation

A novel inhibitor of cyclin-Cdk activity detected in transforming growth factor beta-arrested epithelial cells.

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