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J. Biol. Chem., Vol. 275, Issue 34, 26316-26321, August 25, 2000
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From the Department of Molecular Pathology, Research Institute for
Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi,
Minami-ku, Hiroshima 734-8553, Japan
Members of the SNF2/SWI2 family, characterized
with sequence motifs similar to those found in DNA and RNA helicases,
play roles in various aspects of cellular fundamental processes such as
transcriptional regulation, chromosome stability, nucleotide excision
repair, and recombination. We have isolated a novel member of the human
SNF2/SWI2 family, RAD54B, which is highly homologous to
mammalian RAD54. The RAD54 gene is a member of
the RAD52 epistasis group which is involved in the
recombinational repair of DNA damage. Here we demonstrate that human
Rad54B (hRad54B), like human Rad54 (hRad54), associates with human
Rad51 (hRad51). Both hRad54B and hRad54 associate with hRad51 through
their NH2-terminal domains, but there are differences in
their ways of association with hRad51. In contrast to Rad54, whose
association with Rad51 is induced by ionizing radiation, Rad54B
associates with Rad51 constitutively in immunoprecipitation
experiments. Also, the failure to detect the interaction between
hRad54B and hRad51 in the yeast two-hybrid assay suggests that their
interaction, unlike that between hRad54 and hRad51, may be indirect.
Immunofluorescence microscopy revealed that hRad54B formed nuclear foci
that colocalized with hRad51, hRad54, and BRCA1. These findings suggest
that Rad54B may be functionally distinct from Rad54, although it may
play an active role in recombination processes in concert with other
members of the RAD52 epistasis group.
A Novel Human Rad54 Homologue, Rad54B, Associates with Rad51*
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.: 81-82-257-5828;
Fax: 81-82-256-7102; E-mail: miyag@hiroshima-u.ac.jp.
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