scholarly journals Werner's syndrome protein (WRN) migrates Holliday junctions and co‐localizes with RPA upon replication arrest

EMBO Reports ◽  
2000 ◽  
Vol 1 (1) ◽  
pp. 80-84 ◽  
Author(s):  
Angelos Constantinou ◽  
Madalena Tarsounas ◽  
Julia K Karow ◽  
Robert M Brosh ◽  
Vilhelm A Bohr ◽  
...  
Keyword(s):  
Holliday Junctions ◽  
Werner’S Syndrome ◽  
Replication Arrest ◽  
Werner's Syndrome ◽  
Syndrome Protein

scholarly journals Physical and Functional Interaction between p53 and the Werner’s Syndrome Protein

1999 ◽  
Vol 274 (41) ◽  
pp. 29463-29469 ◽  
Author(s):  
Gil Blander ◽  
Jonathan Kipnis ◽  
Juan Fernando Martinez Leal ◽  
Chang-En Yu ◽  
Gerard D. Schellenberg ◽  
...  
Keyword(s):  
Functional Interaction ◽  
Werner’S Syndrome ◽  
Werner's Syndrome ◽  
Syndrome Protein

scholarly journals Age related expression of Werner's syndrome protein in selected tissues and coexpression of transcription factors

2002 ◽  
Vol 55 (3) ◽  
pp. 195-199 ◽  
Author(s):  
K Motonaga ◽  
M Itoh ◽  
Y Hachiya ◽  
A Endo ◽  
K Kato ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Werner’S Syndrome ◽  
Age Related ◽  
Werner's Syndrome ◽  
Syndrome Protein

scholarly journals Werner's Syndrome Protein Is Required for Correct Recovery after Replication Arrest and DNA Damage Induced in S-Phase of Cell Cycle

2001 ◽  
Vol 12 (8) ◽  
pp. 2412-2421 ◽  
Author(s):  
Pietro Pichierri ◽  
Annapaola Franchitto ◽  
Pasquale Mosesso ◽  
Fabrizio Palitti
Keyword(s):  
Dna Damage ◽  
Replication Fork ◽  
Apoptotic Cell ◽  
Background Level ◽  
Autosomal Recessive Disorder ◽  
S Phase ◽  
Werner’S Syndrome ◽  
Replication Arrest ◽  
Werner's Syndrome ◽  
Cellular Phenotypes

Werner's syndrome (WS) is a rare autosomal recessive disorder that arises as a consequence of mutations in a gene coding for a protein that is a member of RecQ family of DNA helicases, WRN. The cellular function of WRN is still unclear, but on the basis of the cellular phenotypes of WS and of RecQ yeast mutants, its possible role in controlling recombination and/or in maintenance of genomic integrity during S-phase has been envisaged. With the use of two drugs, camptothecin and hydroxyurea, which produce replication-associated DNA damage and/or inhibit replication fork progression, we find that WS cells have a slower rate of repair associated with DNA damage induced in the S-phase and a reduced induction of RAD51 foci. As a consequence, WS cells undergo apoptotic cell death more than normal cells, even if they arrest and resume DNA synthesis at an apparently normal rate. Furthermore, we report that WS cells show a higher background level of DNA strand breaks and an elevated spontaneous induction of RAD51 foci. Our findings support the hypothesis that WRN could be involved in the correct resolution of recombinational intermediates that arise from replication arrest due to either DNA damage or replication fork collapse.

scholarly journals Cigarette Smoke Induces Cellular Senescence via Werner's Syndrome Protein Down-regulation

2009 ◽  
Vol 179 (4) ◽  
pp. 279-287 ◽  
Author(s):  
Toru Nyunoya ◽  
Martha M. Monick ◽  
Aloysius L. Klingelhutz ◽  
Heather Glaser ◽  
Jeffrey R. Cagley ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Cellular Senescence ◽  
Down Regulation ◽  
Werner’S Syndrome ◽  
Werner's Syndrome ◽  
Syndrome Protein
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