Document Detail


Rad54 is dispensable for the ALT pathway.
MedLine Citation:
PMID:  17054727     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Some immortal cells use the alternative lengthening of telomeres (ALT) pathway to maintain their telomeres instead of telomerase. Previous studies revealed that homologous recombination (HR) contributes to the ALT pathway. To further elucidate molecular mechanisms, we inactivated Rad54 involved in HR, in mouse ALT embryonic stem (ES) cells. Although Rad54-deficient ALT ES cells showed radiosensitivity in line with expectation, cell growth and telomeres were maintained for more than 200 cell divisions. Furthermore, although MMC-stimulated sister chromatid exchange (SCE) was suppressed in the Rad54-deficient ALT ES cells, ALT-associated telomere SCE was not affected. This is the first genetic evidence that mouse Rad54 is dispensable for the ALT pathway.
Authors:
Koichi Akiyama; Kosuke Yusa; Hideharu Hashimoto; Anuradha Poonepalli; Manoor Prakash Hande; Naoki Kakazu; Junji Takeda; Makoto Tachibana; Yoichi Shinkai
Related Documents :
6281367 - Control mechanisms governing the infectivity of chlamydia trachomatis for hela cells: m...
22718197 - Rapid image-based cytometry for comparison of fluorescent viability staining methods.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Genes to cells : devoted to molecular & cellular mechanisms     Volume:  11     ISSN:  1356-9597     ISO Abbreviation:  Genes Cells     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-10-23     Completed Date:  2007-02-12     Revised Date:  2010-09-28    
Medline Journal Info:
Nlm Unique ID:  9607379     Medline TA:  Genes Cells     Country:  England    
Other Details:
Languages:  eng     Pagination:  1305-15     Citation Subset:  IM    
Affiliation:
Department of Life Science, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line
Embryonic Stem Cells / metabolism
Mice
Mice, Knockout
Nuclear Proteins / deficiency,  genetics,  metabolism*
Recombination, Genetic
Signal Transduction
Sister Chromatid Exchange
Telomere / metabolism*
Chemical
Reg. No./Substance:
0/Nuclear Proteins; EC 3.6.4.-/Rad54l protein, mouse

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


Previous Document:  Human small G proteins, ObgH1, and ObgH2, participate in the maintenance of mitochondria and nucleol...
Next Document:  Impairment of p38 MAPK-mediated cytosolic phospholipase A2 activation in the kidneys is associated w...