Title |
The radioresistance kinase TLK1B protects the cells by promoting repair of double strand breaks
|
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Published in |
BMC Molecular and Cell Biology, September 2005
|
DOI | 10.1186/1471-2199-6-19 |
Pubmed ID | |
Authors |
Gulshan Sunavala-Dossabhoy, Sri Kripa Balakrishnan, Siddhartha Sen, Sam Nuthalapaty, Arrigo De Benedetti |
Abstract |
The mammalian protein kinase TLK1 is a homologue of Tousled, a gene involved in flower development in Arabidopsis thaliana. The function of TLK1 is not well known, although knockout of the gene in Drosophila or expression of a dominant negative mutant in mouse cells causes loss of nuclear divisions and missegregation of chromosomes probably, due to alterations in chromatin remodeling capacity. Overexpression of TLK1B, a spliced variant of the TLK1 mRNA, in a model mouse cell line increases it's resistance to ionizing radiation (IR) or the radiomimetic drug doxorubicin, also likely due to changes in chromatin remodeling. TLK1B is translationally regulated by the availability of the translation factor eIF4E, and its synthesis is activated by IR. The reason for this mechanism of regulation is likely to provide a rapid means of promoting repair of DSBs. TLK1B specifically phosphorylates histone H3 and Asf1, likely resulting in changes in chromatin structure, particularly at double strand breaks (DSB) sites. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Brazil | 2 | 4% |
France | 1 | 2% |
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Unknown | 49 | 92% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Ph. D. Student | 19 | 36% |
Researcher | 11 | 21% |
Student > Doctoral Student | 5 | 9% |
Student > Master | 5 | 9% |
Professor > Associate Professor | 4 | 8% |
Other | 5 | 9% |
Unknown | 4 | 8% |
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Medicine and Dentistry | 5 | 9% |
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Unknown | 4 | 8% |