Please use this identifier to cite or link to this item: https://doi.org/10.1111/j.1365-2443.2006.01020.x
Title: Rad54 is dispensable for the ALT pathway
Authors: Akiyama, K.
Yusa, K.
Hashimoto, H.
Poonepalli, A. 
Hande, M.P.
Kakazu, N.
Takeda, J.
Tachibana, M.
Shinkai, Y.
Issue Date: Nov-2006
Citation: Akiyama, K., Yusa, K., Hashimoto, H., Poonepalli, A., Hande, M.P., Kakazu, N., Takeda, J., Tachibana, M., Shinkai, Y. (2006-11). Rad54 is dispensable for the ALT pathway. Genes to Cells 11 (11) : 1305-1315. ScholarBank@NUS Repository. https://doi.org/10.1111/j.1365-2443.2006.01020.x
Abstract: 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. © 2006 The AuthorsJournal compilation 2006 by the Molecular Biology Society of Japan/Blackwell Publishing Ltd.
Source Title: Genes to Cells
URI: http://scholarbank.nus.edu.sg/handle/10635/109566
ISSN: 13569597
DOI: 10.1111/j.1365-2443.2006.01020.x
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

7
checked on Nov 30, 2020

WEB OF SCIENCETM
Citations

8
checked on Nov 30, 2020

Page view(s)

76
checked on Nov 28, 2020

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.