PMID- 15013424
OWN - NLM
STAT- MEDLINE
DCOM- 20040409
LR  - 20211203
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 315
IP  - 1
DP  - 2004 Feb 27
TI  - X-ray-induced telomeric instability in Atm-deficient mouse cells.
PG  - 51-8
AB  - The gene responsible for ataxia telangiectasia (AT) encodes ATM protein, which 
      plays a major role in the network of a signal transduction initiated by double 
      strand DNA breaks. To determine how radiation-induced genomic instability is 
      modulated by the dysfunction of ATM protein, we examined radiation-induced 
      delayed chromosomal instability in individual cell lines established from 
      wild-type Atm(+/+), heterozygote Atm(+/-), and knock-out Atm(-/-) mouse embryos. 
      The results indicate that Atm(-/-) mouse cells are highly susceptible to the 
      delayed induction of telomeric instability and end-to-end chromosome fusions by 
      radiation in addition to the elevated spontaneous telomeric instability detected 
      by telomere fluorescence in situ hybridization (FISH). The telomeric instability 
      was characterized by abnormal telomere FISH signals, including loss of the 
      signals and the extra-chromosomal signals that were associated and/or not 
      associated with chromosome ends, suggesting that Atm deficiency makes telomeres 
      vulnerable to breakage. Thus, the present study shows that Atm protein plays an 
      essential role in maintaining telomere integrity and prevents chromosomes from 
      end-to-end fusions, indicating that telomeres are a target for the induction of 
      genomic instability by radiation.
FAU - Undarmaa, Barkhaa
AU  - Undarmaa B
AD  - Laboratory of Radiation Biology, Department of Radiology and Radiation Biology, 
      Course of Life Sciences and Radiation Research, Graduate School of Biomedical 
      Sciences, Nagasaki University, Nagasaki 852-8521, Japan.
FAU - Kodama, Seiji
AU  - Kodama S
FAU - Suzuki, Keiji
AU  - Suzuki K
FAU - Niwa, Otsura
AU  - Niwa O
FAU - Watanabe, Masami
AU  - Watanabe M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
RN  - EC 2.7.11.1 (Atm protein, mouse)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Ataxia Telangiectasia Mutated Proteins
MH  - Cell Cycle Proteins
MH  - Cell Death/radiation effects
MH  - Cell Line
MH  - Chromosome Aberrations/radiation effects
MH  - Cytological Techniques/methods
MH  - DNA-Binding Proteins
MH  - Dose-Response Relationship, Radiation
MH  - Embryo, Mammalian/cytology
MH  - Genomic Instability/physiology
MH  - In Situ Hybridization, Fluorescence
MH  - Mice
MH  - Mice, Inbred C3H
MH  - Mice, Knockout
MH  - Protein Serine-Threonine Kinases/*deficiency/genetics
MH  - Radiation Tolerance
MH  - Telomere/chemistry/*genetics/*radiation effects
MH  - Tumor Suppressor Proteins
MH  - X-Rays/*adverse effects
EDAT- 2004/03/12 05:00
MHDA- 2004/04/10 05:00
CRDT- 2004/03/12 05:00
PHST- 2003/11/01 00:00 [received]
PHST- 2004/03/12 05:00 [pubmed]
PHST- 2004/04/10 05:00 [medline]
PHST- 2004/03/12 05:00 [entrez]
AID - S0006291X04000373 [pii]
AID - 10.1016/j.bbrc.2004.01.014 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2004 Feb 27;315(1):51-8. doi: 
      10.1016/j.bbrc.2004.01.014.