BLM, the Bloom’s syndrome protein, varies during the cell cycle in its amount, distribution, and co-localization with other nuclear proteins

2000 ◽  
Vol 91 (1-4) ◽  
pp. 217-223 ◽  
Author(s):  
M.M. Sanz ◽  
M. Proytcheva ◽  
N.A. Ellis ◽  
W.K. Holloman ◽  
J. German
Oncogene ◽  
2002 ◽  
Vol 21 (13) ◽  
pp. 2079-2088 ◽  
Author(s):  
Mouna Ababou ◽  
Virginie Dumaire ◽  
Yann Lécluse ◽  
Mounira Amor-Guéret

2009 ◽  
Vol 37 (3) ◽  
pp. 553-559 ◽  
Author(s):  
Miranda Payne ◽  
Ian D. Hickson

Bloom's syndrome (BS) is a rare autosomal recessive disorder characterized by genomic instability and cancer predisposition. The underlying genetic defect is mutation of the BLM gene, producing deficiency in the RecQ helicase BLM (Bloom's syndrome protein). The present article begins by introducing BLM and its binding partners before reviewing its known biochemical activities and its potential roles both as a pro-recombinase and as a suppressor of homologous recombination. Finally, the evidence for an emerging role in mitotic chromosome segregation is examined.


Oncogene ◽  
2000 ◽  
Vol 19 (23) ◽  
pp. 2731-2738 ◽  
Author(s):  
Stéphanie Dutertre ◽  
Mouna Ababou ◽  
Rosine Onclercq ◽  
Jozo Delic ◽  
Bruno Chatton ◽  
...  

1998 ◽  
Vol 18 (5) ◽  
pp. 2721-2728 ◽  
Author(s):  
Scott Davey ◽  
Christine S. Han ◽  
Sarah A. Ramer ◽  
Jennifer C. Klassen ◽  
Adam Jacobson ◽  
...  

ABSTRACT The human BLM gene is a member of the Escherichia coli recQ helicase family, which includes the Saccharomyces cerevisiae SGS1 and human WRN genes. Defects inBLM are responsible for the human disease Bloom’s syndrome, which is characterized in part by genomic instability and a high incidence of cancer. Here we describe the cloning ofrad12 +, which is the fission yeast homolog ofBLM and is identical to the recently reportedrhq1 + gene. We showed that rad12null cells are sensitive to DNA damage induced by UV light and γ radiation, as well as to the DNA synthesis inhibitor hydroxyurea. Overexpression of the wild-type rad12 + gene also leads to sensitivity to these agents and to defects associated with the loss of the S-phase and G2-phase checkpoint control. We showed genetically and biochemically thatrad12 + acts upstream fromrad9 +, one of the fission yeast G2checkpoint control genes, in regulating exit from the S-phase checkpoint. The physical chromosome segregation defects seen inrad12 null cells combined with the checkpoint regulation defect seen in the rad12 + overproducer implicate rad12 + as a key coupler of chromosomal integrity with cell cycle progression.


2017 ◽  
Vol 26 (8) ◽  
pp. 088701
Author(s):  
Zhen-Ye Zhao ◽  
Chun-Hua Xu ◽  
Jing Shi ◽  
Jing-Hua Li ◽  
Jian-Bing Ma ◽  
...  

2003 ◽  
Vol 279 (11) ◽  
pp. 9847-9856 ◽  
Author(s):  
Sudha Sharma ◽  
Joshua A. Sommers ◽  
Leonard Wu ◽  
Vilhelm A. Bohr ◽  
Ian D. Hickson ◽  
...  

2005 ◽  
Vol 24 (7) ◽  
pp. 1465-1476 ◽  
Author(s):  
Jinhu Yin ◽  
Alexandra Sobeck ◽  
Chang Xu ◽  
Amom Ruhikanta Meetei ◽  
Maureen Hoatlin ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document