scholarly journals Rapamycin (sirolimus) inhibits proliferating cell nuclear antigen expression and blocks cell cycle in the G1 phase in human keratinocyte stem cells.

1997 ◽  
Vol 99 (9) ◽  
pp. 2094-2099 ◽  
Author(s):  
A F Javier ◽  
Z Bata-Csorgo ◽  
C N Ellis ◽  
S Kang ◽  
J J Voorhees ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Nuclear Antigen ◽  
G1 Phase ◽  
Human Keratinocyte ◽  
Proliferating Cell ◽  
Keratinocyte Stem Cells

Requirement for proliferating cell nuclear antigen expression during stages of the Chinese hamster ovary cell cycle

Biochemistry ◽  
1989 ◽  
Vol 28 (7) ◽  
pp. 2967-2974 ◽  
Author(s):  
Yin Chang Liu ◽  
Robert L. Marraccino ◽  
Peter C. Keng ◽  
Robert A. Bambara ◽  
Edith M. Lord ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Chinese Hamster Ovary Cell ◽  
Chinese Hamster Ovary ◽  
Proliferating Cell Nuclear Antigen ◽  
Chinese Hamster ◽  
Antigen Expression ◽  
Ovary Cell ◽  
Nuclear Antigen ◽  
Proliferating Cell

scholarly journals Chromatin Bound PCNA is Complexed with Cell Cycle Protein Regulators as Determined by Chromatin Immunoprecipitation

2017 ◽  
Vol 56 (1) ◽  
Author(s):  
Nazul Becerril ◽  
Miguel Ángel Martínez ◽  
Elpidio García ◽  
Jorge Manuel Vázquez Ramos
Keyword(s):  
Cell Cycle ◽  
Chromatin Immunoprecipitation ◽  
Proliferating Cell Nuclear Antigen ◽  
Nuclear Antigen ◽  
G1 Phase ◽  
Cell Cycle Protein ◽  
Protein Targets ◽  
Maize Seeds ◽  
Proliferating Cell ◽  
Formation Of Complexes

Using the technique of Chromatin Immunoprecipitation, we have detected the formation of complexes between the homotrimer protein ring Proliferating Cell Nuclear Antigen, PCNA, and two fundamental regulators of the cell cycle, CdkA and Cyclin D4;2 along germination of maize seeds. This finding suggests the way PCNA participates in the control of the G1 phase, by allowing cyclin-kinase complexes to find and phosphorylate protein targets. Incidentally, PCNA may form a structure of a dimer of trimer when bound to the chromatin.

Demonstration of cell cycle kinetics in thyroid primary culture by immunostaining of proliferating cell nuclear antigen: differences in cyclic AMP-dependent and -independent mitogenic stimulations

1993 ◽  
Vol 105 (1) ◽  
pp. 69-80 ◽  
Author(s):  
M. Baptist ◽  
J.E. Dumont ◽  
P.P. Roger
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Primary Culture ◽  
Proliferating Cell Nuclear Antigen ◽  
Cell Cycle Progression ◽  
Nuclear Antigen ◽  
Major Influence ◽  
Cell Cycle Kinetics ◽  
Experimental Conditions ◽  
Proliferating Cell

In this study, experimental conditions are described that allowed us to follow the fate of the DNA polymerase delta-associated proliferating cell nuclear antigen (PCNA), by immunolabeling during the overall cell cycle. Differences in subcellular localization or the presence of PCNA allowed us to identify each phase of the cell cycle. Using these cell cycle markers in dog thyroid epithelial cells in primary culture, we found unexpected differences in cell cycle kinetics, in response to stimulations through cAMP-dependent and cAMP-independent pathways. These provide a new dimension to the view that the two pathways are largely separate, but co-operate on DNA synthesis initiation. More precisely, thyrotropin (TSH), acting via cAMP, exerts a potent triggering effect on DNA synthesis, associated with a precocious induction of PCNA appearance. This constitutes the major influence of TSH (cAMP) in determining cell cycle progression, which is only partly moderated by TSH-dependent lengthening of S- and G2-phases.

The Impact of 5-Azacytidine on Placental Weight, Glycoprotein Pattern and Proliferating Cell Nuclear Antigen Expression in Rat Placenta

Placenta ◽  
2007 ◽  
Vol 28 (8-9) ◽  
pp. 803-811 ◽  
Author(s):  
L. Šerman ◽  
M. Vlahović ◽  
M. Šijan ◽  
F. Bulić-Jakuš ◽  
A. Šerman ◽  
...  
Keyword(s):  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Placental Weight ◽  
Nuclear Antigen ◽  
The Impact ◽  
Proliferating Cell

scholarly journals An evaluation of antioxidant effects on recovery from postischemic acute renal failure.

1994 ◽  
Vol 4 (8) ◽  
pp. 1588-1597
Author(s):  
R A Zager ◽  
S M Fuerstenberg ◽  
P H Baehr ◽  
D Myerson ◽  
B Torok-Storb
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Dna Fragmentation ◽  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Nuclear Antigen ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tubular Necrosis ◽  
Proliferating Cell

Xanthine oxidase (XO) activity and hydroxyl radical (.OH) formation are widely proposed mediators of renal reperfusion injury, potentially altering the severity of, and recovery from, postischemic acute renal failure. The goal of this study was to ascertain whether combination XO inhibitor (oxypurinol) and .OH scavenger (Na benzoate) therapy, given at the time of renal ischemia, alters the extent of: (1) tubular necrosis and filtration failure; (2) DNA fragmentation/apoptosis (assessed in situ by terminal deoxynucleotidyl transferase reactivity); (3) early tubular regenerative responses (proliferating cell nuclear antigen expression; (3H)thymidine incorporation); and (4) the rate and/or degree of functional and morphologic repair. The effects of XO inhibition, .OH scavengers, and "catalytic" iron (FeSO4) on human proximal tubular cell proliferation in vitro were also assessed with a newly established cell line (HK-2). Male Sprague-Dawley rats were subjected to 35 min of bilateral renal arterial occlusion with or without oxypurinol/benzoate therapy. These agents did not alter the extent of tubular necrosis or filtration failure, proliferating cell nuclear antigen expression or thymidine incorporation, or the rate/extent of renal functional/morphologic repair. DNA fragmentation did not precede tubular necrosis, and it was unaffected by antioxidant therapy. By 5 days postischemia, both treatment groups demonstrated regenerating epithelial fronds that protruded into the lumina. These structures contained terminal deoxynucleotidyl transferase-reactive, but morphologically intact, cells, suggesting the presence of apoptosis. Oxypurinol and .OH scavengers (benzoate; dimethylthiourea) suppressed in vitro tubular cell proliferation; conversely, catalytic Fe had a growth-stimulatory effect. These results suggest that: (1) XO inhibition/.OH scavenger therapy has no discernible net effect on postischemic acute renal failure; (2) DNA fragmentation does not precede tubular necrosis, suggesting that it is not a primary mediator of ischemic cell death; and (3) antioxidants can be antiproliferative for human tubular cells, possibly mitigating their potential beneficial effects.

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