scholarly journals DNA damage-induced CHK1 autophosphorylation at Ser296 is regulated by an intramolecular mechanism

FEBS Letters ◽  
2012 ◽  
Vol 586 (22) ◽  
pp. 3974-3979 ◽  
Author(s):  
Naoyuki Okita ◽  
Shota Minato ◽  
Eri Ohmi ◽  
Sei-ichi Tanuma ◽  
Yoshikazu Higami
2005 ◽  
Vol 187 (16) ◽  
pp. 5624-5630 ◽  
Author(s):  
Barbara C. McCabe ◽  
David R. Pawlowski ◽  
Gerald B. Koudelka

ABSTRACT Inactivation of the lambdoid phage repressor protein is necessary to induce lytic growth of a lambdoid prophage. Activated RecA, the mediator of the host SOS response to DNA damage, causes inactivation of the repressor by stimulating the repressor's nascent autocleavage activity. The repressor of bacteriophage lambda and its homolog, LexA, preferentially undergo RecA-stimulated autocleavage as free monomers, which requires that each monomer mediates its own (intramolecular) cleavage. The cI repressor of bacteriophage 434 preferentially undergoes autocleavage as a dimer specifically bound to DNA, opening the possibility that one 434 repressor subunit may catalyze proteolysis of its partner subunit (intermolecular cleavage) in the DNA-bound dimer. Here, we first identified and mutagenized the residues at the cleavage and active sites of 434 repressor. We utilized the mutant repressors to show that the DNA-bound 434 repressor dimer overwhelmingly prefers to use an intramolecular mechanism of autocleavage. Our data suggest that the 434 repressor cannot be forced to use an intermolecular cleavage mechanism. Based on these data, we propose a model in which the cleavage-competent conformation of the repressor is stabilized by operator binding.


2004 ◽  
Vol 171 (4S) ◽  
pp. 416-416
Author(s):  
Tamer M. Said ◽  
Shyam Allamaneni ◽  
Kiran P. Nallella ◽  
Rakesh K. Sharma ◽  
Sijo J. Parekattil ◽  
...  

Nature ◽  
2020 ◽  
Vol 579 (7800) ◽  
pp. 499-500
Author(s):  
Irene Gallina ◽  
Julien P. Duxin
Keyword(s):  

1999 ◽  
Vol 96 (1) ◽  
pp. 143-146 ◽  
Author(s):  
J.-P. Pouget ◽  
J.-L. Ravanat ◽  
T. Douki ◽  
M.-J. Richard ◽  
J. Cadet

2010 ◽  
Vol 49 (S 01) ◽  
pp. S64-S68
Author(s):  
E. Dikomey

SummaryIonising irradiation acts primarily via induction of DNA damage, among which doublestrand breaks are the most important lesions. These lesions may lead to lethal chromosome aberrations, which are the main reason for cell inactivation. Double-strand breaks can be repaired by several different mechanisms. The regulation of these mechanisms appears be fairly different for normal and tumour cells. Among different cell lines capacity of doublestrand break repair varies by only few percents and is known to be determined mostly by genetic factors. Knowledge about doublestrand break repair mechanisms and their regulation is important for the optimal application of ionising irradiation in medicine.


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