| Cell cycle checkpoints: the role and evaluation for early diagnosis of senescence, cardiovascular, cancer, and neurodegenerative diseases. | |
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MedLine Citation:
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PMID: 17136506 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Maintenance of genomic integrity is critical for prevention of a wide variety of adverse cellular effects including apoptosis, cellular senescence, and malignant cell transformation. Under stress conditions and even during an unperturbed cell cycle, checkpoint proteins play the key role in genome maintenance by and mediating cellular response to DNA damage, and represent an essential part of the "cellular stress response proteome". Intact checkpoint signal transduction cascades check the presence of genome damage, trigger cell cycle arrest, and forward the information to the protein core of cell cycle machinery, replication apparatus, repair, and/or apoptotic protein cores. Genetic checkpoint defects lead to syndromes that demonstrate chromosomal instability, increased sensitivity to genotoxic stress, tissue degeneration, developmental retardation, premature aging, and cancer predisposition that is most extensively studied for the ATM-checkpoint mutated in Ataxia telangiectasia. Tissue specific epigenetic control over the function of cell cycle checkpoints can be, further, misregulated by aberrant DNA methylation status. The consequent checkpoint dysregulation may result in tissue specific degenerative processes such as degeneration and calcification of heart aortic valves, diabetic cardiomyopathy, hyperhomocysteinemic cerebrovascular, peripheral vascular and coronary heart diseases, neurodegenerative disorders (Alzheimer and Parkinson diseases, amyotrophic lateral sclerosis, glaucoma), and accelerated aging frequently accompanied with cancer. This review focuses on the checkpoints shown to be crucial for unperturbed cell cycle regulation, dysregulation of which might be considered as a potential molecular marker for early diagnosis of and therapy efficiency in neurodegenerative, cardiovascular and cancer diseases. An application of the most potent detection technologies such as "Disease Proteomics and Transcriptomics" also considered here, allows a most specific selection of diagnostic markers. |
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Authors:
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O Golubnitschaja |
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Publication Detail:
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Type: Journal Article; Review Date: 2006-11-30 |
Journal Detail:
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Title: Amino acids Volume: 32 ISSN: 0939-4451 ISO Abbreviation: Amino Acids Publication Date: 2007 |
Date Detail:
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Created Date: 2007-04-09 Completed Date: 2007-09-14 Revised Date: 2011-11-02 |
Medline Journal Info:
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Nlm Unique ID: 9200312 Medline TA: Amino Acids Country: Austria |
Other Details:
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Languages: eng Pagination: 359-71 Citation Subset: IM |
Affiliation:
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Department of Radiology, Friedrich-Wilhelms-University of Bonn, Bonn, Germany. Olga.Golubnitschaja@ukb.uni-bonn.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Calcinosis / diagnosis, metabolism Cardiovascular Diseases / diagnosis*, metabolism*, therapy Cell Aging* Cell Cycle* Cell Cycle Proteins / metabolism Cell Transformation, Neoplastic / metabolism DNA Damage DNA Methylation DNA Repair DNA Replication DNA-Binding Proteins / metabolism Diagnosis, Differential Epigenesis, Genetic Genome, Human Humans Neoplasms / diagnosis*, metabolism*, therapy Neurodegenerative Diseases / diagnosis*, metabolism*, therapy Protein-Serine-Threonine Kinases / metabolism Proteome / metabolism Tumor Markers, Biological / metabolism* Tumor Suppressor Proteins / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/Proteome; 0/Tumor Markers, Biological; 0/Tumor Suppressor Proteins; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/ataxia telangiectasia mutated protein |
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