Document Detail


Adenosine induces G2/M cell-cycle arrest by inhibiting cell mitosis progression.
MedLine Citation:
PMID:  19947935     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cellular adenosine accumulates under stress conditions. Few papers on adenosine are concerned with its function in the cell cycle. The cell cycle is the essential mechanism by which all living things reproduce and the target machinery when cells encounter stresses, so it is necessary to examine the relationship between adenosine and the cell cycle. In the present study, adenosine was found to induce G-2/M cell-cycle arrest. Furthermore, adenosine was found to modulate the expression of some important proteins in the cell cycle, such as cyclin B and p21, and to inhibit the transition of metaphase to anaphase in mitosis.
Authors:
Kun-Zhi Jia; Bo Tang; Lu Yu; Wei Cheng; Rong Zhang; Jian-Fa Zhang; Zi-Chun Hua
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-12-16
Journal Detail:
Title:  Cell biology international     Volume:  34     ISSN:  1095-8355     ISO Abbreviation:  Cell Biol. Int.     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2009-12-16     Completed Date:  2010-05-04     Revised Date:  2010-11-12    
Medline Journal Info:
Nlm Unique ID:  9307129     Medline TA:  Cell Biol Int     Country:  England    
Other Details:
Languages:  eng     Pagination:  49-52     Citation Subset:  IM    
Affiliation:
Jiangsu Center of Hepatobiliary Diseases, State Key Laboratory of Pharmaceutical Biotechnology, Affiliated Gulou Hospital, Nanjing University, Nanjing 210093, People's Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Adenosine / pharmacology*
Anaphase
Cell Division
Cell Line
Cyclin B / metabolism
Cyclin-Dependent Kinase Inhibitor p21 / metabolism
Flow Cytometry
G2 Phase
Humans
Metaphase
Microscopy, Fluorescence
Mitosis*
Chemical
Reg. No./Substance:
0/Cyclin B; 0/Cyclin-Dependent Kinase Inhibitor p21; 58-61-7/Adenosine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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