NFBD1/MDC1 participates in the regulation of G2/M transition in mammalian cells
NFBD1/MDC1 is a large nuclear protein involved in the early cellular response to DNA damage. Upon DNA damage, NFBD1 has an ability to facilitate the efficient DNA repair. In the present study, we have found that, in addition to DNA damage response, NFBD1 plays a critical role in the regulation of G2...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2010-06, Vol.397 (2), p.157-162 |
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| container_title | Biochemical and biophysical research communications |
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| creator | Bu, Youquan Suenaga, Yusuke Okoshi, Rintaro Sang, Meixiang Kubo, Natsumi Song, Fangzhou Nakagawara, Akira Ozaki, Toshinori |
| description | NFBD1/MDC1 is a large nuclear protein involved in the early cellular response to DNA damage. Upon DNA damage, NFBD1 has an ability to facilitate the efficient DNA repair. In the present study, we have found that, in addition to DNA damage response, NFBD1 plays a critical role in the regulation of G2/M transition. Expression study using synchronized HeLa cells demonstrated that, like the mitotic kinase Plk1, NFBD1 expression level is maximal in G2/M-phase of the cell cycle. siRNA-mediated knockdown of NFBD1 resulted in G2/M arrest as well as simultaneous apoptosis in association with a significant increase in the amounts of γH2AX and pro-apoptotic p73. Since a remarkable down-regulation of mitotic phospho-histone H3 was detectable in NFBD1-knocked down cells, it is likely that knocking down of NFBD1 inhibits G2/M transition. Taken together, our present findings suggest that NFBD1 has a pivotal role in the regulation of proper mitotic entry. |
| doi_str_mv | 10.1016/j.bbrc.2010.05.063 |
| format | Article |
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Upon DNA damage, NFBD1 has an ability to facilitate the efficient DNA repair. In the present study, we have found that, in addition to DNA damage response, NFBD1 plays a critical role in the regulation of G2/M transition. Expression study using synchronized HeLa cells demonstrated that, like the mitotic kinase Plk1, NFBD1 expression level is maximal in G2/M-phase of the cell cycle. siRNA-mediated knockdown of NFBD1 resulted in G2/M arrest as well as simultaneous apoptosis in association with a significant increase in the amounts of γH2AX and pro-apoptotic p73. Since a remarkable down-regulation of mitotic phospho-histone H3 was detectable in NFBD1-knocked down cells, it is likely that knocking down of NFBD1 inhibits G2/M transition. Taken together, our present findings suggest that NFBD1 has a pivotal role in the regulation of proper mitotic entry.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2010.05.063</identifier><identifier>PMID: 20529673</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; APOPTOSIS ; Apoptosis - genetics ; CELL CYCLE ; Cell cycle arrest ; Cell Division - genetics ; DNA DAMAGES ; DNA REPAIR ; DNA-Binding Proteins - metabolism ; G2 Phase - genetics ; Gene Knockdown Techniques ; GENE REGULATION ; HELA CELLS ; Humans ; Mitosis - genetics ; NFBD1 ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Nuclear Proteins - physiology ; p73 ; PROTEINS ; RNA, Small Interfering - genetics ; siRNA ; Trans-Activators - genetics ; Trans-Activators - physiology ; Tumor Protein p73 ; Tumor Suppressor Proteins - metabolism</subject><ispartof>Biochemical and biophysical research communications, 2010-06, Vol.397 (2), p.157-162</ispartof><rights>2010 Elsevier Inc.</rights><rights>Copyright (c) 2010 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-6a2417fe1cb49383585b14769e8295a75720ae07f4fe580b8a05b1a5ac22e4093</citedby><cites>FETCH-LOGICAL-c449t-6a2417fe1cb49383585b14769e8295a75720ae07f4fe580b8a05b1a5ac22e4093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X1000954X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20529673$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22202656$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Bu, Youquan</creatorcontrib><creatorcontrib>Suenaga, Yusuke</creatorcontrib><creatorcontrib>Okoshi, Rintaro</creatorcontrib><creatorcontrib>Sang, Meixiang</creatorcontrib><creatorcontrib>Kubo, Natsumi</creatorcontrib><creatorcontrib>Song, Fangzhou</creatorcontrib><creatorcontrib>Nakagawara, Akira</creatorcontrib><creatorcontrib>Ozaki, Toshinori</creatorcontrib><title>NFBD1/MDC1 participates in the regulation of G2/M transition in mammalian cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>NFBD1/MDC1 is a large nuclear protein involved in the early cellular response to DNA damage. Upon DNA damage, NFBD1 has an ability to facilitate the efficient DNA repair. In the present study, we have found that, in addition to DNA damage response, NFBD1 plays a critical role in the regulation of G2/M transition. Expression study using synchronized HeLa cells demonstrated that, like the mitotic kinase Plk1, NFBD1 expression level is maximal in G2/M-phase of the cell cycle. siRNA-mediated knockdown of NFBD1 resulted in G2/M arrest as well as simultaneous apoptosis in association with a significant increase in the amounts of γH2AX and pro-apoptotic p73. Since a remarkable down-regulation of mitotic phospho-histone H3 was detectable in NFBD1-knocked down cells, it is likely that knocking down of NFBD1 inhibits G2/M transition. Taken together, our present findings suggest that NFBD1 has a pivotal role in the regulation of proper mitotic entry.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>APOPTOSIS</subject><subject>Apoptosis - genetics</subject><subject>CELL CYCLE</subject><subject>Cell cycle arrest</subject><subject>Cell Division - genetics</subject><subject>DNA DAMAGES</subject><subject>DNA REPAIR</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>G2 Phase - genetics</subject><subject>Gene Knockdown Techniques</subject><subject>GENE REGULATION</subject><subject>HELA CELLS</subject><subject>Humans</subject><subject>Mitosis - genetics</subject><subject>NFBD1</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Nuclear Proteins - physiology</subject><subject>p73</subject><subject>PROTEINS</subject><subject>RNA, Small Interfering - genetics</subject><subject>siRNA</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - physiology</subject><subject>Tumor Protein p73</subject><subject>Tumor Suppressor Proteins - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLJDEUhYM4aOv4B1xIgQtX1X2TSlIVcKPta6B73MyAu5BK39I09WiTtDD_flK2unR14fKdw-Ej5JTClAKVs_W0rr2dMkgPEFOQxR6ZUFCQMwp8n0wAQOZM0adDchTCGoBSLtUBOWQgmJJlMSGPv--ub-hseTOn2cb46KzbmIghc30WXzDz-LxtTXRDnw1Nds9myyx60wf3_kpQZ7rOtM70mcW2DT_Jj8a0AU8-7jH5e3f7Z_6QLx7vf82vFrnlXMVcGsZp2SC1NVdFVYhK1JSXUmHFlDClKBkYhLLhDYoK6spAAowwljHkoIpjcr7rHUJ0OlgX0b7Yoe_RRs0YAyaFTNTFjtr44XWLIerOhXGn6XHYBl0WhRRFYhPJdqT1QwgeG73xrjP-n6agR9t6rUfberStQehkO4XOPuq3dYerr8in3gRc7gBMKt4c-nEp9hZXzo9DV4P7rv8_MQSNNA</recordid><startdate>20100625</startdate><enddate>20100625</enddate><creator>Bu, Youquan</creator><creator>Suenaga, Yusuke</creator><creator>Okoshi, Rintaro</creator><creator>Sang, Meixiang</creator><creator>Kubo, Natsumi</creator><creator>Song, Fangzhou</creator><creator>Nakagawara, Akira</creator><creator>Ozaki, Toshinori</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20100625</creationdate><title>NFBD1/MDC1 participates in the regulation of G2/M transition in mammalian cells</title><author>Bu, Youquan ; 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Upon DNA damage, NFBD1 has an ability to facilitate the efficient DNA repair. In the present study, we have found that, in addition to DNA damage response, NFBD1 plays a critical role in the regulation of G2/M transition. Expression study using synchronized HeLa cells demonstrated that, like the mitotic kinase Plk1, NFBD1 expression level is maximal in G2/M-phase of the cell cycle. siRNA-mediated knockdown of NFBD1 resulted in G2/M arrest as well as simultaneous apoptosis in association with a significant increase in the amounts of γH2AX and pro-apoptotic p73. Since a remarkable down-regulation of mitotic phospho-histone H3 was detectable in NFBD1-knocked down cells, it is likely that knocking down of NFBD1 inhibits G2/M transition. 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| ispartof | Biochemical and biophysical research communications, 2010-06, Vol.397 (2), p.157-162 |
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| subjects | 60 APPLIED LIFE SCIENCES APOPTOSIS Apoptosis - genetics CELL CYCLE Cell cycle arrest Cell Division - genetics DNA DAMAGES DNA REPAIR DNA-Binding Proteins - metabolism G2 Phase - genetics Gene Knockdown Techniques GENE REGULATION HELA CELLS Humans Mitosis - genetics NFBD1 Nuclear Proteins - genetics Nuclear Proteins - metabolism Nuclear Proteins - physiology p73 PROTEINS RNA, Small Interfering - genetics siRNA Trans-Activators - genetics Trans-Activators - physiology Tumor Protein p73 Tumor Suppressor Proteins - metabolism |
| title | NFBD1/MDC1 participates in the regulation of G2/M transition in mammalian cells |
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