Newly identified structurally disparate modulators of osmosensitive taurine efflux inhibit cell cycle progression

Abstract We identified an allele of Saccharomyces cerevisiae CDC20 that exhibits a spindle-assembly checkpoint defect. Previous studies indicated that loss of CDC20 function caused cell cycle arrest prior to the onset of anaphase. In contrast, CDC20-50 caused inappropriate cell cycle progression through M phase in the absence of mitotic spindle function. This effect of CDC20-50 was dominant over wild type and was eliminated by a second mutation causing loss of function, suggesting that it encodes an overactive form of Cdc20p. Overexpression of CDC20 was found to cause a similar checkpoint defect, causing bypass of the preanaphase arrest produced by either microtubule-depolymerizing compounds or MPS1 overexpression. CDC20 overexpression was also able to overcome the anaphase delay caused by high levels of the anaphase inhibitor Pds1p, but not a mutant form immune to anaphase-promoting complex- (APC-)mediated proteolysis. CDC20 overexpression was unable to promote anaphase in cells deficient in APC function. These findings suggest that Cdc20p is a limiting factor that promotes anaphase entry by antagonizing Pds1p. Cdc20p may promote the APC-dependent proteolytic degradation of Pds1p and other factors that act to inhibit cell cycle progression through mitosis.

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Free fatty acids trigger apoptosis and inhibit cell cycle progression in human vascular endothelial cells

The FASEB Journal ◽

10.1096/fj.03-0301fje ◽

2003 ◽

Vol 18 (1) ◽

pp. 146-148 ◽

Cited By ~ 111

Author(s):

Michaela Artwohl ◽

Michael Roden ◽

Werner Waldhäusl ◽

Angelika Freudenthaler ◽

Sabina M. Baumgartner‐Parzer

Keyword(s):

Cell Cycle ◽

Fatty Acids ◽

Endothelial Cells ◽

Free Fatty Acids ◽

Cell Cycle Progression ◽

Vascular Endothelial Cells ◽

Vascular Endothelial ◽

Cycle Progression ◽

Inhibit Cell Cycle Progression

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Unique natural antioxidants (NAOs) and derived purified components inhibit cell cycle progression by downregulation of ppRb and E2F in human PC3 prostate cancer cells

FEBS Letters ◽

10.1016/j.febslet.2004.06.101 ◽

2004 ◽

Vol 573 (1-3) ◽

pp. 31-37 ◽

Cited By ~ 10

Author(s):

Shlomo Bakshi ◽

Margalit Bergman ◽

Sara Dovrat ◽

Shlomo Grossman

Keyword(s):

Prostate Cancer ◽

Cell Cycle ◽

Cancer Cells ◽

Cell Cycle Progression ◽

Natural Antioxidants ◽

Prostate Cancer Cells ◽

Cycle Progression ◽

Inhibit Cell Cycle Progression

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Diarsenic and tetraarsenic oxide inhibit cell cycle progression and bFGF- and VEGF-induced proliferation of human endothelial cells

Journal of Cellular Biochemistry ◽

10.1002/jcb.20329 ◽

2005 ◽

Vol 95 (1) ◽

pp. 120-130 ◽

Cited By ~ 24

Author(s):

Sang Hyeok Woo ◽

Myung-Jin Park ◽

Sungkwan An ◽

Hyung-Chahn Lee ◽

Hyeon-Ok Jin ◽

...

Keyword(s):

Cell Cycle ◽

Endothelial Cells ◽

Cell Cycle Progression ◽

Human Endothelial Cells ◽

Cycle Progression ◽

Inhibit Cell Cycle Progression

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Regulation of vascular smooth muscle cell proliferation by plasma membrane Ca(2+)-ATPase

AJP Cell Physiology ◽

10.1152/ajpcell.1997.272.6.c1947 ◽

1997 ◽

Vol 272 (6) ◽

pp. C1947-C1959 ◽

Cited By ~ 50

Author(s):

M. Husain ◽

L. Jiang ◽

V. See ◽

K. Bein ◽

M. Simons ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Smooth Muscle ◽

Plasma Membrane ◽

Vascular Smooth Muscle ◽

Cell Cycle Progression ◽

Critical Role ◽

Cycle Progression ◽

Inhibit Cell Cycle Progression ◽

Transient Overexpression

We have previously shown that reductions in c-Myb-dependent transcription inhibit cell cycle progression and decrease intracellular Ca2+ concentrations in vascular smooth muscle cells (VSMC). We now report that these effects are largely mediated by a 4- to 10-fold increased rate of La(3+)-sensitive 45Ca extrusion, which is associated with 2- to 4-fold increased levels of plasma membrane Ca(2+)-ATPase 1 (PMCA1) mRNA and protein. PMCA4 mRNA, present at much lower concentrations, undergoes similar changes during suppression of c-Myb activity. We also report that PMCA1 expression is regulated during VSMC cell cycle progression, such that levels of PMCA1 are 40% lower at the G1/S interface than at G0. Moreover, transient overexpression of PMCA1a in VSMC elevates the 45Ca efflux rate by approximately 2-fold, decreases resting and peak thapsigargin-releasable Ca2+ concentrations at G1/S by 43% (68 nM) and 52% (160 nM), respectively, and reduces the rate of cell proliferation by over 2.5-fold. These data define a mechanism for c-Myb-dependent Ca2+ homeostasis and support a critical role for PMCA in the regulation of VSMC growth.

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