scholarly journals Characterizing the DNA damage response in putative stem cells of resected normal lung and matched NSCLC patient samples

2017 ◽  
Vol 28 ◽  
pp. ii4
Author(s):  
T.M. Marti ◽  
C.C. Tièche ◽  
R. Peng ◽  
S.R.R. Hall ◽  
L. Froment ◽  
...  
2018 ◽  
Vol 24 (24) ◽  
pp. 6583-6593 ◽  
Author(s):  
Peter W. Nagle ◽  
Nynke A. Hosper ◽  
Lara Barazzuol ◽  
Anne L. Jellema ◽  
Mirjam Baanstra ◽  
...  

Author(s):  
Maria Louka ◽  
Effrossyni Boutou ◽  
Vasiliki Bakou ◽  
Vassiliki Pappa ◽  
Anastasios Georgoulis ◽  
...  

2016 ◽  
Vol 186 (1) ◽  
pp. 17-26 ◽  
Author(s):  
Kalpana Mujoo ◽  
E. Brian Butler ◽  
Raj K. Pandita ◽  
Clayton R. Hunt ◽  
Tej K. Pandita

2013 ◽  
Vol 6 (259) ◽  
pp. ra5-ra5 ◽  
Author(s):  
J. Carreras Puigvert ◽  
L. von Stechow ◽  
R. Siddappa ◽  
A. Pines ◽  
M. Bahjat ◽  
...  

2012 ◽  
Vol 46 (1) ◽  
pp. 30-42 ◽  
Author(s):  
Mangmang Li ◽  
Yunlong He ◽  
Wendy Dubois ◽  
Xiaolin Wu ◽  
Jianxin Shi ◽  
...  

2015 ◽  
Vol 208 (5) ◽  
pp. 513-520 ◽  
Author(s):  
Jianhua Xiong ◽  
Dilyana Todorova ◽  
Ning-Yuan Su ◽  
Jinchul Kim ◽  
Pei-Jen Lee ◽  
...  

Mouse embryonic stem cells (ESCs) are genetically more stable than somatic cells, thereby preventing the passage of genomic abnormalities to their derivatives including germ cells. The underlying mechanisms, however, remain largely unclear. In this paper, we show that the stemness factor Sall4 is required for activating the critical Ataxia Telangiectasia Mutated (ATM)–dependent cellular responses to DNA double-stranded breaks (DSBs) in mouse ESCs and confer their resistance to DSB-induced cytotoxicity. Sall4 is rapidly mobilized to the sites of DSBs after DNA damage. Furthermore, Sall4 interacts with Rad50 and stabilizes the Mre11–Rad50–Nbs1 complex for the efficient recruitment and activation of ATM. Sall4 also interacts with Baf60a, a member of the SWI/SNF (switch/sucrose nonfermentable) ATP-dependent chromatin-remodeling complex, which is responsible for recruiting Sall4 to the site of DNA DSB damage. Our findings provide novel mechanisms to coordinate stemness of ESCs with DNA damage response, ensuring genomic stability during the expansion of ESCs.


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