Cell Cycle Control by Ataxia Telangiectasia Mutated Protein Through Regulating Retinoblastoma Protein Phosphorylation

2012 ◽  
pp. 103-115
Author(s):  
Javier G. Pizarro ◽  
Antoni Camins ◽  
Felix Junyent ◽  
Ester Verdaguer ◽  
Carme Auladell ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Protein Phosphorylation ◽  
Ataxia Telangiectasia ◽  
Cell Cycle Control ◽  
Retinoblastoma Protein ◽  
Ataxia Telangiectasia Mutated ◽  
Ataxia Telangiectasia Mutated Protein

ATM is involved in cell-cycle control through the regulation of retinoblastoma protein phosphorylation

2010 ◽  
pp. n/a-n/a ◽  
Author(s):  
Javier G. Pizarro ◽  
Jaume Folch ◽  
Aurelio Vazquez de la Torre ◽  
Felix Junyent ◽  
Ester Verdaguer ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Protein Phosphorylation ◽  
Cell Cycle Control ◽  
Retinoblastoma Protein

A multifaceted role for ATM in genome maintenance

2003 ◽  
Vol 5 (16) ◽  
pp. 1-21 ◽  
Author(s):  
Tej K. Pandita
Keyword(s):  
Cell Cycle ◽  
Ataxia Telangiectasia ◽  
Cell Cycle Control ◽  
Cell Cycle Checkpoints ◽  
Telomere Maintenance ◽  
Loss Of Function ◽  
Genome Maintenance ◽  
Ataxia Telangiectasia Mutated ◽  
Gonadal Atrophy ◽  
Mitogenic Signal Transduction

The pleiotropic nature of the clinical phenotypes of patients with ataxia-telangiectasia (A-T) – which encompass cerebellar degeneration (leading to ataxia), gonadal atrophy, and cancer predisposition – suggests multiple functions of the gene responsible for the disease. The ataxia-telangiectasia mutated gene product (ATM), whose loss of function is responsible for ataxia-telangiectasia, is a protein kinase that interacts with several substrates and is implicated in mitogenic signal transduction, chromosome condensation, meiotic recombination, cell-cycle control and telomere maintenance. This review focuses on the critical roles that ATM appears to play in cell-cycle checkpoints, DNA repair, telomere metabolism and oxidative stress, indicating how defects in these processes might lead to ataxia-telangiectasia.

Targeting the Ataxia Telangiectasia Mutated Protein in Cancer Therapy

2016 ◽  
Vol 17 (2) ◽  
pp. 139-153 ◽  
Author(s):  
Donatella Vecchio ◽  
Guido Frosina
Keyword(s):  
Cancer Therapy ◽  
Ataxia Telangiectasia ◽  
Ataxia Telangiectasia Mutated ◽  
Ataxia Telangiectasia Mutated Protein

Retinoblastoma Protein, Gene Expression, and Cell Cycle Control

Cancer Genes ◽  
1996 ◽  
pp. 177-191
Author(s):  
Jane Clifford Azizkhan ◽  
Shiaw Yih Lin ◽  
David Jensen ◽  
Dusan Kostic ◽  
Adrian R. Black
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Protein Gene ◽  
Cell Cycle Control ◽  
Retinoblastoma Protein

scholarly journals Ataxia-Telangiectasia-Mutated Protein Expression as a Prognostic Marker in Adenoid Cystic Carcinoma of the Salivary Glands

2018 ◽  
Vol 59 (6) ◽  
pp. 717
Author(s):  
Shadavlonjid Bazarsad ◽  
Jue Young Kim ◽  
Xianglan Zhang ◽  
Ki-Yeol Kim ◽  
Doo Young Lee ◽  
...  
Keyword(s):  
Protein Expression ◽  
Adenoid Cystic Carcinoma ◽  
Salivary Glands ◽  
Prognostic Marker ◽  
Ataxia Telangiectasia ◽  
Ataxia Telangiectasia Mutated ◽  
Adenoid Cystic ◽  
Ataxia Telangiectasia Mutated Protein

Integration of cell cycle control with transcriptional regulation by the retinoblastoma protein

1993 ◽  
Vol 5 (2) ◽  
pp. 194-200 ◽  
Author(s):  
Robert E. Hollingsworth ◽  
Phang-Lang Chen ◽  
Wen-Hwa Lee
Keyword(s):  
Cell Cycle ◽  
Transcriptional Regulation ◽  
Cell Cycle Control ◽  
Retinoblastoma Protein

ATR (ataxia telangiectasia mutated- and Rad3-related kinase) is activated by mild hypothermia in mammalian cells and subsequently activates p53

2011 ◽  
Vol 435 (2) ◽  
pp. 499-508 ◽  
Author(s):  
Anne Roobol ◽  
Jo Roobol ◽  
Martin J. Carden ◽  
Amandine Bastide ◽  
Anne E. Willis ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ataxia Telangiectasia ◽  
Mammalian Cells ◽  
Mild Hypothermia ◽  
Chinese Hamster ◽  
Membrane Lipid ◽  
Mitogen Activated Protein Kinase ◽  
Ataxia Telangiectasia Mutated ◽  
Mitogen Activated Protein

In vitro cultured mammalian cells respond to mild hypothermia (27–33 °C) by attenuating cellular processes and slowing and arresting the cell cycle. The slowing of the cell cycle at the upper range (31–33 °C) and its complete arrest at the lower range (27–28 °C) of mild hypothermia is effected by the activation of p53 and subsequent expression of p21. However, the mechanism by which cold is perceived in mammalian cells with the subsequent activation of p53 has remained undetermined. In the present paper, we report that the exposure of Chinese-hamster ovary-K1 cells to mildly hypothermic conditions activates the ATR (ataxia telangiectasia mutated- and Rad3-related kinase)–p53–p21 signalling pathway and is thus a key pathway involved in p53 activation upon mild hypothermia. In addition, we show that although p38MAPK (p38 mitogen-activated protein kinase) is also involved in activation of p53 upon mild hypothermia, this is probably the result of activation of p38MAPK by ATR. Furthermore, we show that cold-induced changes in cell membrane lipid composition are correlated with the activation of the ATR–p53–p21 pathway. Therefore we provide the first mechanistic detail of cell sensing and signalling upon mild hypothermia in mammalian cells leading to p53 and p21 activation, which is known to lead to cell cycle arrest.

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