Please use this identifier to cite or link to this item:
|Title:||Rad54 is dispensable for the ALT pathway||Authors:||Akiyama, K.
|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.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.