Evaluation of γ-radiation-induced DNA damage in two species of bivalves and their relative sensitivity using comet assay

2014 ◽  
Vol 150 ◽  
pp. 1-8 ◽  
Author(s):  
M.K. Praveen Kumar ◽  
S.K. Shyama ◽  
B.S. Sonaye ◽  
U Roshini Naik ◽  
S.B. Kadam ◽  
...  
2002 ◽  
Vol 43 (2) ◽  
pp. 153-153 ◽  
Author(s):  
REMA RAJAGOPALAN ◽  
KHALIDA WANI ◽  
NAGARAJ G. HUILGOL ◽  
TSUTOMU V. KAGIYA ◽  
CHERUPALLY K. KRISHNAN NAIR

Oncogene ◽  
2006 ◽  
Vol 26 (16) ◽  
pp. 2365-2373 ◽  
Author(s):  
A M Ghaleb ◽  
J P Katz ◽  
K H Kaestner ◽  
J X Du ◽  
V W Yang

Blood ◽  
2000 ◽  
Vol 95 (8) ◽  
pp. 2645-2650 ◽  
Author(s):  
Lisa A. Porter ◽  
Gurmit Singh ◽  
Jonathan M. Lee

Abstract γ-Radiation is a potent inducer of apoptosis. There are multiple pathways regulating DNA damage-induced apoptosis, and we set out to identify novel mechanisms regulating γ-radiation–induced apoptosis in hematopoietic cells. In this report, we present data implicating the cyclin B1 protein as a regulator of apoptotic fate following DNA damage. Cyclin B1 is the regulatory subunit of the cdc2 serine/threonine kinase, and accumulation of cyclin B1 in late G2 phase of the cell cycle is a prerequisite for mitotic initiation in mammalian cells. We find that abundance of the cyclin B1 protein rapidly increases in several mouse and human hematopoietic cells (Ramos, DP16, HL60, thymocytes) undergoing γ-radiation–induced apoptosis. Cyclin B1 accumulation occurs in all phases of the cell cycle. Antisense inhibition of cyclin B1 accumulation decreases apoptosis, and ectopic cyclin B1 expression is sufficient to induce apoptosis. These observations are consistent with the idea that cyclin B1 is both necessary and sufficient for γ-radiation-induced apoptosis.


2003 ◽  
Vol 65 (4) ◽  
pp. 471-477 ◽  
Author(s):  
Seiichi WADA ◽  
Hidemitsu KURAHAYASHI ◽  
Yasuhiko KOBAYASHI ◽  
Tomoo FUNAYAMA ◽  
Kazuo YAMAMOTO ◽  
...  

1990 ◽  
Vol 122 (1) ◽  
pp. 86 ◽  
Author(s):  
Peggy L. Olive ◽  
Judit P. Banáth ◽  
Ralph E. Durand ◽  
Judit P. Banath

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