hCAS / CSE 1L regulates RAD 51 distribution and focus formation for homologous recombinational repair
Homologous recombinational repair ( HR ) is one of the major repair systems for DNA double‐strand breaks. RAD 51 is a key molecule in HR , and the RAD 51 concentration in the cell nucleus increases after DNA damage induction. However, the mechanism that regulates the intracellular distribution of RA...
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| Veröffentlicht in: | Genes to cells : devoted to molecular & cellular mechanisms 2015-09, Vol.20 (9), p.681-694 |
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| container_title | Genes to cells : devoted to molecular & cellular mechanisms |
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| creator | Okimoto, Satoshi Sun, Jiying Fukuto, Atsuhiko Horikoshi, Yasunori Matsuda, Shun Matsuda, Tomonari Ikura, Masae Ikura, Tsuyoshi Machida, Shinichi Kurumizaka, Hitoshi Miyamoto, Yoichi Oka, Masahiro Yoneda, Yoshihiro Kiuchi, Yoshiaki Tashiro, Satoshi |
| description | Homologous recombinational repair (
HR
) is one of the major repair systems for
DNA
double‐strand breaks.
RAD
51 is a key molecule in
HR
, and the
RAD
51 concentration in the cell nucleus increases after
DNA
damage induction. However, the mechanism that regulates the intracellular distribution of
RAD
51 is still unclear. Here, we show that
hCAS
/
CSE
1L associates with
RAD
51 in human cells. We found that
hCAS
/
CSE
1L negatively regulates the nuclear protein level of
RAD
51 under normal conditions.
hCAS
/
CSE
1L is also required to repress the
DNA
damage‐induced focus formation of
RAD
51. Moreover, we show that
hCAS
/
CSE
1L plays roles in the regulation of the
HR
activity and in chromosome stability. These findings suggest that
hCAS
/
CSE
1L is responsible for controlling the
HR
activity by directly interacting with
RAD
51. |
| doi_str_mv | 10.1111/gtc.12262 |
| format | Article |
| fullrecord | <record><control><sourceid>crossref</sourceid><recordid>TN_cdi_crossref_primary_10_1111_gtc_12262</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>10_1111_gtc_12262</sourcerecordid><originalsourceid>FETCH-LOGICAL-c742-8112af73b00490e97402c69b29db0b82e0b60b1e4f331a9871395363227c99963</originalsourceid><addsrcrecordid>eNotkDFPwzAQhS0EEqUw8A-8MqT12bETj1UoBSkSEu0e2Y6TGiVxZScD_540cMO7d-9JN3wIPQPZwDzbdjQboFTQG7QCJnhC05TdXj0XieQyu0cPMX4TAowSvkL2XOyOeIuL4x5DiYNtp06NNuKv3SvmgGsXx-D0NDo_YDXUuPFmirOGXi3Z7PDZ977zrZ-LYI3vtRuWUnXzfVEuPKK7RnXRPv3vNTq97U_Fe1J-Hj6KXZmYLKVJDkBVkzFNSCqJlVlKqBFSU1lronNqiRZEg00bxkDJPAMmOROM0sxIKQVbo5e_tyb4GINtqktwvQo_FZDqiqea8VQLHvYLKFVWYA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>hCAS / CSE 1L regulates RAD 51 distribution and focus formation for homologous recombinational repair</title><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Wiley Free Content</source><creator>Okimoto, Satoshi ; Sun, Jiying ; Fukuto, Atsuhiko ; Horikoshi, Yasunori ; Matsuda, Shun ; Matsuda, Tomonari ; Ikura, Masae ; Ikura, Tsuyoshi ; Machida, Shinichi ; Kurumizaka, Hitoshi ; Miyamoto, Yoichi ; Oka, Masahiro ; Yoneda, Yoshihiro ; Kiuchi, Yoshiaki ; Tashiro, Satoshi</creator><creatorcontrib>Okimoto, Satoshi ; Sun, Jiying ; Fukuto, Atsuhiko ; Horikoshi, Yasunori ; Matsuda, Shun ; Matsuda, Tomonari ; Ikura, Masae ; Ikura, Tsuyoshi ; Machida, Shinichi ; Kurumizaka, Hitoshi ; Miyamoto, Yoichi ; Oka, Masahiro ; Yoneda, Yoshihiro ; Kiuchi, Yoshiaki ; Tashiro, Satoshi</creatorcontrib><description>Homologous recombinational repair (
HR
) is one of the major repair systems for
DNA
double‐strand breaks.
RAD
51 is a key molecule in
HR
, and the
RAD
51 concentration in the cell nucleus increases after
DNA
damage induction. However, the mechanism that regulates the intracellular distribution of
RAD
51 is still unclear. Here, we show that
hCAS
/
CSE
1L associates with
RAD
51 in human cells. We found that
hCAS
/
CSE
1L negatively regulates the nuclear protein level of
RAD
51 under normal conditions.
hCAS
/
CSE
1L is also required to repress the
DNA
damage‐induced focus formation of
RAD
51. Moreover, we show that
hCAS
/
CSE
1L plays roles in the regulation of the
HR
activity and in chromosome stability. These findings suggest that
hCAS
/
CSE
1L is responsible for controlling the
HR
activity by directly interacting with
RAD
51.</description><identifier>ISSN: 1356-9597</identifier><identifier>EISSN: 1365-2443</identifier><identifier>DOI: 10.1111/gtc.12262</identifier><language>eng</language><ispartof>Genes to cells : devoted to molecular & cellular mechanisms, 2015-09, Vol.20 (9), p.681-694</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c742-8112af73b00490e97402c69b29db0b82e0b60b1e4f331a9871395363227c99963</citedby><cites>FETCH-LOGICAL-c742-8112af73b00490e97402c69b29db0b82e0b60b1e4f331a9871395363227c99963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids></links><search><creatorcontrib>Okimoto, Satoshi</creatorcontrib><creatorcontrib>Sun, Jiying</creatorcontrib><creatorcontrib>Fukuto, Atsuhiko</creatorcontrib><creatorcontrib>Horikoshi, Yasunori</creatorcontrib><creatorcontrib>Matsuda, Shun</creatorcontrib><creatorcontrib>Matsuda, Tomonari</creatorcontrib><creatorcontrib>Ikura, Masae</creatorcontrib><creatorcontrib>Ikura, Tsuyoshi</creatorcontrib><creatorcontrib>Machida, Shinichi</creatorcontrib><creatorcontrib>Kurumizaka, Hitoshi</creatorcontrib><creatorcontrib>Miyamoto, Yoichi</creatorcontrib><creatorcontrib>Oka, Masahiro</creatorcontrib><creatorcontrib>Yoneda, Yoshihiro</creatorcontrib><creatorcontrib>Kiuchi, Yoshiaki</creatorcontrib><creatorcontrib>Tashiro, Satoshi</creatorcontrib><title>hCAS / CSE 1L regulates RAD 51 distribution and focus formation for homologous recombinational repair</title><title>Genes to cells : devoted to molecular & cellular mechanisms</title><description>Homologous recombinational repair (
HR
) is one of the major repair systems for
DNA
double‐strand breaks.
RAD
51 is a key molecule in
HR
, and the
RAD
51 concentration in the cell nucleus increases after
DNA
damage induction. However, the mechanism that regulates the intracellular distribution of
RAD
51 is still unclear. Here, we show that
hCAS
/
CSE
1L associates with
RAD
51 in human cells. We found that
hCAS
/
CSE
1L negatively regulates the nuclear protein level of
RAD
51 under normal conditions.
hCAS
/
CSE
1L is also required to repress the
DNA
damage‐induced focus formation of
RAD
51. Moreover, we show that
hCAS
/
CSE
1L plays roles in the regulation of the
HR
activity and in chromosome stability. These findings suggest that
hCAS
/
CSE
1L is responsible for controlling the
HR
activity by directly interacting with
RAD
51.</description><issn>1356-9597</issn><issn>1365-2443</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNotkDFPwzAQhS0EEqUw8A-8MqT12bETj1UoBSkSEu0e2Y6TGiVxZScD_540cMO7d-9JN3wIPQPZwDzbdjQboFTQG7QCJnhC05TdXj0XieQyu0cPMX4TAowSvkL2XOyOeIuL4x5DiYNtp06NNuKv3SvmgGsXx-D0NDo_YDXUuPFmirOGXi3Z7PDZ977zrZ-LYI3vtRuWUnXzfVEuPKK7RnXRPv3vNTq97U_Fe1J-Hj6KXZmYLKVJDkBVkzFNSCqJlVlKqBFSU1lronNqiRZEg00bxkDJPAMmOROM0sxIKQVbo5e_tyb4GINtqktwvQo_FZDqiqea8VQLHvYLKFVWYA</recordid><startdate>201509</startdate><enddate>201509</enddate><creator>Okimoto, Satoshi</creator><creator>Sun, Jiying</creator><creator>Fukuto, Atsuhiko</creator><creator>Horikoshi, Yasunori</creator><creator>Matsuda, Shun</creator><creator>Matsuda, Tomonari</creator><creator>Ikura, Masae</creator><creator>Ikura, Tsuyoshi</creator><creator>Machida, Shinichi</creator><creator>Kurumizaka, Hitoshi</creator><creator>Miyamoto, Yoichi</creator><creator>Oka, Masahiro</creator><creator>Yoneda, Yoshihiro</creator><creator>Kiuchi, Yoshiaki</creator><creator>Tashiro, Satoshi</creator><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>201509</creationdate><title>hCAS / CSE 1L regulates RAD 51 distribution and focus formation for homologous recombinational repair</title><author>Okimoto, Satoshi ; Sun, Jiying ; Fukuto, Atsuhiko ; Horikoshi, Yasunori ; Matsuda, Shun ; Matsuda, Tomonari ; Ikura, Masae ; Ikura, Tsuyoshi ; Machida, Shinichi ; Kurumizaka, Hitoshi ; Miyamoto, Yoichi ; Oka, Masahiro ; Yoneda, Yoshihiro ; Kiuchi, Yoshiaki ; Tashiro, Satoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c742-8112af73b00490e97402c69b29db0b82e0b60b1e4f331a9871395363227c99963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okimoto, Satoshi</creatorcontrib><creatorcontrib>Sun, Jiying</creatorcontrib><creatorcontrib>Fukuto, Atsuhiko</creatorcontrib><creatorcontrib>Horikoshi, Yasunori</creatorcontrib><creatorcontrib>Matsuda, Shun</creatorcontrib><creatorcontrib>Matsuda, Tomonari</creatorcontrib><creatorcontrib>Ikura, Masae</creatorcontrib><creatorcontrib>Ikura, Tsuyoshi</creatorcontrib><creatorcontrib>Machida, Shinichi</creatorcontrib><creatorcontrib>Kurumizaka, Hitoshi</creatorcontrib><creatorcontrib>Miyamoto, Yoichi</creatorcontrib><creatorcontrib>Oka, Masahiro</creatorcontrib><creatorcontrib>Yoneda, Yoshihiro</creatorcontrib><creatorcontrib>Kiuchi, Yoshiaki</creatorcontrib><creatorcontrib>Tashiro, Satoshi</creatorcontrib><collection>CrossRef</collection><jtitle>Genes to cells : devoted to molecular & cellular mechanisms</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Okimoto, Satoshi</au><au>Sun, Jiying</au><au>Fukuto, Atsuhiko</au><au>Horikoshi, Yasunori</au><au>Matsuda, Shun</au><au>Matsuda, Tomonari</au><au>Ikura, Masae</au><au>Ikura, Tsuyoshi</au><au>Machida, Shinichi</au><au>Kurumizaka, Hitoshi</au><au>Miyamoto, Yoichi</au><au>Oka, Masahiro</au><au>Yoneda, Yoshihiro</au><au>Kiuchi, Yoshiaki</au><au>Tashiro, Satoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>hCAS / CSE 1L regulates RAD 51 distribution and focus formation for homologous recombinational repair</atitle><jtitle>Genes to cells : devoted to molecular & cellular mechanisms</jtitle><date>2015-09</date><risdate>2015</risdate><volume>20</volume><issue>9</issue><spage>681</spage><epage>694</epage><pages>681-694</pages><issn>1356-9597</issn><eissn>1365-2443</eissn><abstract>Homologous recombinational repair (
HR
) is one of the major repair systems for
DNA
double‐strand breaks.
RAD
51 is a key molecule in
HR
, and the
RAD
51 concentration in the cell nucleus increases after
DNA
damage induction. However, the mechanism that regulates the intracellular distribution of
RAD
51 is still unclear. Here, we show that
hCAS
/
CSE
1L associates with
RAD
51 in human cells. We found that
hCAS
/
CSE
1L negatively regulates the nuclear protein level of
RAD
51 under normal conditions.
hCAS
/
CSE
1L is also required to repress the
DNA
damage‐induced focus formation of
RAD
51. Moreover, we show that
hCAS
/
CSE
1L plays roles in the regulation of the
HR
activity and in chromosome stability. These findings suggest that
hCAS
/
CSE
1L is responsible for controlling the
HR
activity by directly interacting with
RAD
51.</abstract><doi>10.1111/gtc.12262</doi><tpages>14</tpages></addata></record> |
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| ispartof | Genes to cells : devoted to molecular & cellular mechanisms, 2015-09, Vol.20 (9), p.681-694 |
| issn | 1356-9597 1365-2443 |
| language | eng |
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| source | Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Free Content |
| title | hCAS / CSE 1L regulates RAD 51 distribution and focus formation for homologous recombinational repair |
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