scholarly journals Solution Structure of Human Growth Arrest and DNA Damage 45α (Gadd45α) and Its Interactions with Proliferating Cell Nuclear Antigen (PCNA) and Aurora A Kinase

2010 ◽  
Vol 285 (29) ◽  
pp. 22196-22201 ◽  
Author(s):  
Ricardo Sánchez ◽  
David Pantoja-Uceda ◽  
Jesús Prieto ◽  
Tammo Diercks ◽  
María J. Marcaida ◽  
...  
2011 ◽  
Vol 23 (2) ◽  
pp. 806-822 ◽  
Author(s):  
Alessandra Amoroso ◽  
Lorenzo Concia ◽  
Caterina Maggio ◽  
Cécile Raynaud ◽  
Catherine Bergounioux ◽  
...  

APOPTOSIS ◽  
2009 ◽  
Vol 14 (3) ◽  
pp. 268-275 ◽  
Author(s):  
Xiang He ◽  
Congwen Wei ◽  
Ting Song ◽  
Jing Yuan ◽  
Yanhong Zhang ◽  
...  

2005 ◽  
Vol 118 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Taichi Yamamoto ◽  
Yoko Mori ◽  
Toyotaka Ishibashi ◽  
Yukinobu Uchiyama ◽  
Tadamasa Ueda ◽  
...  

2010 ◽  
Vol 285 (13) ◽  
pp. 10044-10052 ◽  
Author(s):  
Da-Qiang Li ◽  
Suresh B. Pakala ◽  
Sirigiri Divijendra Natha Reddy ◽  
Kazufumi Ohshiro ◽  
Shao-Hua Peng ◽  
...  

2010 ◽  
Vol 38 (1) ◽  
pp. 104-109 ◽  
Author(s):  
Alfonso Gallego-Sánchez ◽  
Francisco Conde ◽  
Pedro San Segundo ◽  
Avelino Bueno

Eukaryotes ubiquitylate the replication factor PCNA (proliferating-cell nuclear antigen) so that it tolerates DNA damage. Although, in the last few years, the understanding of the evolutionarily conserved mechanism of ubiquitylation of PCNA, and its crucial role in DNA damage tolerance, has progressed impressively, little is known about the deubiquitylation of this sliding clamp in most organisms. In the present review, we will discuss potential molecular mechanisms regulating PCNA deubiquitylation in yeast.


2000 ◽  
Vol 275 (49) ◽  
pp. 38261-38267 ◽  
Author(s):  
Brian K. Law ◽  
Mary E. Waltner-Law ◽  
Amelia J. Entingh ◽  
Anna Chytil ◽  
Mary E. Aakre ◽  
...  

1999 ◽  
Vol 19 (1) ◽  
pp. 12-20 ◽  
Author(s):  
Jin Xu ◽  
Gilbert F. Morris

ABSTRACT The proliferating cell nuclear antigen (PCNA) is a highly conserved cellular protein that functions both in DNA replication and in DNA repair. Exposure of a rat embryo fibroblast cell line (CREF cells) to γ radiation induced simultaneous expression of PCNA with the p53 tumor suppressor protein and the cyclin-dependent kinase inhibitor p21WAF1/Cip1. PCNA mRNA levels transiently increased in serum-starved cells exposed to ionizing radiation, an observation suggesting that the radiation-associated increase in PCNA expression could be dissociated from cell cycle progression. Irradiation of CREF cells activated a transiently expressed PCNA promoter chloramphenicol acetyltransferase construct through p53 binding sequences via a mechanism blocked by a dominant negative mutant p53. Electrophoretic mobility shift assays with nuclear extracts prepared from irradiated CREF cells produced four p53-specific DNA-protein complexes with the PCNA p53 binding site. Addition of monoclonal antibody PAb421 (p53-specific) or AC238 (specific to the transcriptional coactivator p300/CREB binding protein) to the mobility shift assay distinguished different forms of p53 that changed in relative abundance with time after irradiation. These findings suggest a complex cellular response to DNA damage in which p53 transiently activates expression of PCNA for the purpose of limited DNA repair. In a population of nongrowing cells with diminished PCNA levels, this pathway may be crucial to survival following DNA damage.


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