Catalase inhibition in diabetic rats potentiates DNA damage and apoptotic cell death setting the stage for cardiomyopathy

2014 ◽  
Vol 70 (4) ◽  
pp. 947-959 ◽  
Author(s):  
Svetlana Ivanović-Matić ◽  
Desanka Bogojević ◽  
Vesna Martinović ◽  
Anja Petrović ◽  
Sofija Jovanović-Stojanov ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Diabetic Rats ◽  
Apoptotic Cell Death ◽  
Catalase Inhibition

scholarly journals RUNX Family Participates in the Regulation of p53-Dependent DNA Damage Response

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Toshinori Ozaki ◽  
Akira Nakagawara ◽  
Hiroki Nagase
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Dna Damage Response ◽  
Apoptotic Cell ◽  
Genetic Alterations ◽  
Apoptotic Cell Death ◽  
Cycle Arrest ◽  
Damage Response

A proper DNA damage response (DDR), which monitors and maintains the genomic integrity, has been considered to be a critical barrier against genetic alterations to prevent tumor initiation and progression. The representative tumor suppressor p53 plays an important role in the regulation of DNA damage response. When cells receive DNA damage, p53 is quickly activated and induces cell cycle arrest and/or apoptotic cell death through transactivating its target genes implicated in the promotion of cell cycle arrest and/or apoptotic cell death such asp21WAF1,BAX, andPUMA. Accumulating evidence strongly suggests that DNA damage-mediated activation as well as induction of p53 is regulated by posttranslational modifications and also by protein-protein interaction. Loss of p53 activity confers growth advantage and ensures survival in cancer cells by inhibiting apoptotic response required for tumor suppression. RUNX family, which is composed of RUNX1, RUNX2, and RUNX3, is a sequence-specific transcription factor and is closely involved in a variety of cellular processes including development, differentiation, and/or tumorigenesis. In this review, we describe a background of p53 and a functional collaboration between p53 and RUNX family in response to DNA damage.

scholarly journals Treadmill exercise ameliorates apoptotic cell death in the retinas of diabetic rats

2013 ◽  
Vol 7 (6) ◽  
pp. 1745-1750 ◽  
Author(s):  
DAE-YOUNG KIM ◽  
SUN-YOUNG JUNG ◽  
CHANG-JU KIM ◽  
YUN-HEE SUNG ◽  
JAE-DEUNG KIM
Keyword(s):  
Cell Death ◽  
Treadmill Exercise ◽  
Apoptotic Cell ◽  
Diabetic Rats ◽  
Apoptotic Cell Death

scholarly journals An age-related increase in resistance to DNA damage-induced apoptotic cell death is associated with development of DNA repair mechanisms

2003 ◽  
Vol 84 (6) ◽  
pp. 1275-1287 ◽  
Author(s):  
Alejandro A. Romero ◽  
Stephane R. Gross ◽  
Ke-Yi Cheng ◽  
Noriko K. Goldsmith ◽  
Herbert M. Geller
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Dna Repair ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Dna Repair Mechanisms ◽  
Age Related ◽  
Repair Mechanisms ◽  
Related Increase

Oral administration of Cr(VI) induced oxidative stress, DNA damage and apoptotic cell death in mice

Toxicology ◽  
2006 ◽  
Vol 228 (1) ◽  
pp. 16-23 ◽  
Author(s):  
Xiao-Feng Wang ◽  
Ming-Luan Xing ◽  
Ying Shen ◽  
Xin Zhu ◽  
Li-Hong Xu
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Cell Death ◽  
Oral Administration ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death
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