The Werner and Bloom syndrome proteins catalyze regression of a model replication fork.
Biochemistry
; 45(47): 13939-46, 2006 Nov 28.
Article
em En
| MEDLINE
| ID: mdl-17115688
ABSTRACT
The premature aging and cancer-prone diseases Werner and Bloom syndromes are caused by loss of function of WRN and BLM proteins, respectively. At the cellular level, WRN or BLM deficiency causes replication abnormalities, DNA damage hypersensitivity, and genome instability, suggesting that these proteins might participate in resolution of replication blockage. Although WRN and BLM are helicases belonging to the RecQ family, both have been recently shown to also facilitate pairing of complementary DNA strands. In this study, we demonstrate that both WRN and BLM (but not other selected helicases) can coordinate their unwinding and pairing activities to regress a model replication fork substrate. Notably, fork regression is widely believed to be the initial step in responding to replication blockage. Our findings suggest that WRN and/or BLM might regress replication forks in vivo as part of a genome maintenance pathway, consistent with the phenotypes of WRN- and BLM-deficient cells.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Adenosina Trifosfatases
/
DNA Helicases
/
Replicação do DNA
/
RecQ Helicases
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Revista:
Biochemistry
Ano de publicação:
2006
Tipo de documento:
Article