The proto-oncogene c-myb mediates an intracellular calcium rise during the late G1 phase of the cell cycle.

Simons, Michael; Morgan, K. G.; Parker, C.; Collins, Elliott J.; Rosenberg, Robert D.

doi:10.1016/s0021-9258(18)54197-1

Cited by 35 publications

(2 citation statements)

References 28 publications

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“…Over the past 20 years, data has accumulated, from many sources, that both c-fos and c-jun proteins (components of AP-1 transcription factor) are critically involved in the mediation of nuclear events provoked by numerous stimuli [83][84][85][86][87][172][173][174]. The protooncogenes c-fos and c-jun are known to participate in numerous pathophysiological processes including signal transduction, cell growth, differentiation, and cell transformation [83][84][85][86][87].…”

Section: Mechanisms By Which Paf and Paf-rs Function In Vsm Cells: Roles Of Nf-kb Proto-oncogenes Mg 2+ Phenotypic Changes And Vascular mentioning

confidence: 99%

“…Almost 30 years ago, two of us reported, for the first time, the importance of the endothelial lining of blood vessels in the responses of arterial muscles to reduced levels of [Mg 2+ ] 0 [180]. More recently this work has been expanded by our laboratory and others [167][168][169][170][171][172][173][174][175][176][177][178][179][180][181], reinforcing the roles of Mg in control of the microcirculation, blood pressure, distribution of blood flow, inflammation and herogenesis [4,14,15,17,18,19,20,25,29,34,49,53,59,68,74,77,78,79]. We have found, as stated above, that short-term MgD causes marked reductions in the cardiovascular tissue/cell levels of the free radical scavenger glutathione (which is correlated with reduced Mg levels) coupled to fragmentation of DNA (and oxidation) and activation of diverse nitric oxide synthases [15, 25, 81, 82, 89, 90, 91, 93-95, 97-99, 150].…”

Section: Low Mg Paf Telomerase Activity and Agingmentioning

confidence: 99%

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The Expression of Platelet-Activating Factor is Induced by Low Extracellular Mg2+ in Aortic, Cerebral and Neonatal Coronary Vascular Smooth Muscle; Cross Talk with Ceramide Production, NF–kB and Proto-Oncogenes: Possible Links to Atherogenesis and Sudden Cardiac Death in Children and Infants, and Aging; Hypothesis, Review and Viewpoint

Bm¹,

Li²,

Zhang³

et al. 2016

IJCRR

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An attempt is made, herein, to reconcile, and integrate, various phenomena associated with magnesium deficiency (MgD) in cardiovascular health, disease, and aging as well as reasons for the high incidence of sudden cardiac death in infants and young adults. With new experiments, we demonstrate, for the first time, that very low concentrations of platelet-activating factor (PAF), when added to primary cultured cerebral, neonatal coronary, and aortic vascular smooth muscle (VSM) cells (from three different mammals) promote rapid rises in free intracellular Ca 2+ ions and a significant, concomitant reduction in free intracellular Mg 2+ ions; these actions of PAF being curtailed with a specific membrane-receptor inhibitor of PAF.Our new experiments also demonstrate that addition of PAF to the VSM cells result in activation of NF-kB, activation of the proto-oncogenes c-fos and c-jun, a generation/release of ceramide, and synthesis of DNA; most of these actions being inhibited by a specific membrane-receptor antagonist of PAF. In addition, we show, for the first time, formation of 4-hydroxy-2-nonenal (4-HNE) in VSM cells incubated in Mg-deficient (MgD) environments or after addition of PAF. This is important because 4-HNE is a well-known inducer of hydrogen peroxide, known to be formed in MgD VSM cells and that 4-HNE is known to induce DNA damage and fragmentation, events that we have shown previously in VSM and cardiac muscle cells exposed to low Mg environments. Lastly, our experiments demonstrate that incubation of cerebral, neonatal coronary and aortic VSM cells in low Mg 2+ induces: 1. rapid formation of PAF which can be attenuated greatly with a specific membrane-receptor antagonist of PAF; and 2. rises in cellular levels of ceramide, NF-kB activation and formation of the proto-oncogenes, and synthesis of DNA, all of which could be inhibited with a specific membrane-receptor antagonist of PAF. These new findings suggest major roles for PAF (and probably PAF-like lipids) and ceramide formation in the cardiovascular manifestations of MgD, inflammation, atherogenesis, aging, and sudden cardiac death in children. The significance of our new findings are reviewed in light of other works on MgD, inflammation, atherogenesis, sudden cardiac death, and aging.

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Section: Mechanisms By Which Paf and Paf-rs Function In Vsm Cells: Roles Of Nf-kb Proto-oncogenes Mg 2+ Phenotypic Changes And Vascular mentioning

confidence: 99%

Section: Low Mg Paf Telomerase Activity and Agingmentioning

confidence: 99%

The Expression of Platelet-Activating Factor is Induced by Low Extracellular Mg2+ in Aortic, Cerebral and Neonatal Coronary Vascular Smooth Muscle; Cross Talk with Ceramide Production, NF–kB and Proto-Oncogenes: Possible Links to Atherogenesis and Sudden Cardiac Death in Children and Infants, and Aging; Hypothesis, Review and Viewpoint

Bm¹,

Li²,

Zhang³

et al. 2016

IJCRR

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Flow cytometric study of changes in the intracellular free calcium during the cell cycle

1996

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We measured the intracellular levels of free cytoplasmic calcium in different phases of the cell cycle in viable rat fibroblasts, using two parameter flow cytometric analysis with Hoechst 33342 as the DNA specific dye and Fluo‐3 as the calcium sensitive dye. We studied changes in calcium levels during the G1 phase of cell cycle by arresting cells with chemical agents such as staurosporine and hydroxyurea or by density dependent arrest of cell growth. We show that levels of calcium are lowest at the beginning of G1 phase but rise steadily with its progression and culminate at the G1/S border. Our results suggest that complex changes occur in calcium levels during the process of mitotic division. During progression of S and G2 phases, calcium levels decline and increase respectively. Our results offer a new methodology to estimate intracellular calcium levels in specific phases of the cell cycle. Based upon these results we propose a general scheme representing the changes in the intracellular calcium concentration during the progression of the cell cycle. © 1996 Wiley‐Liss, Inc.

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c-Myb function in fibroblasts

et al. 1997

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The protooncogene c-myb is a nuclear transcription factor that shares significant sequence homology with two other myb family members, A-myb and B-myb. Recent studies have suggested that c-myb is involved in regulation of the cell cycle via control of intracellular calcium [Ca2+]i concentration. Given the limited cell type expression of the c-myb gene, we set out to investigate whether myb-dependent cell cycle regulation occurs in cells not known to express the c-myb protein. NIH 3T3 fibroblasts were stably transfected with an inducible c-myb dominant negative construct composed of a myb DNA binding domain linked to the Drosophila engrailed transcription suppresser (pGREMEn) and a full-length murine c-myb cDNA sequence. Induced expression of the dominant negative construct was associated with a G1 cell cycle arrest and a failure to increase late G1 intracellular calcium levels. Similar expression studies in mouse embryonic fibroblasts derived from the c-myb knockout mouse have demonstrated lower baseline [Ca2+]i levels than in normal mice fibroblasts that were not further lowered by MEn expression. We conclude that regulation of calcium homeostasis and cell cycle progression via myb-dependent transcription may play an important role in cells not possessing detectable levels of c-myb protein.

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The proto-oncogene c-myb mediates an intracellular calcium rise during the late G1 phase of the cell cycle.

Cited by 35 publications

References 28 publications

Flow cytometric study of changes in the intracellular free calcium during the cell cycle

c-Myb function in fibroblasts

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