絞り込み

16640

広告

ダビンチ没後500年記念 最大規模の特別展 仏ルーブル美術館

ルネサンスの巨匠、レオナルド・ダビンチの没後500年を記念して、世界中からダビンチやその弟子たちの作品を集めた過去最大規模の特別展が、24日からフランスのルーブ...

  1. [企業] Provention Bio社...
  2. クルド人はどんな人たち? 4カ国に暮らす...
  3. インフルエンザ新防御機構を東大が解明、効...
  4. ニホンザル 餌を得るため2匹が協力 初め...

ニュース一覧

BLM and the FANC proteins collaborate in a common pathway in response to stalled replication forks.

著者 Pichierri P , Franchitto A , Rosselli F
EMBO J.2004 Aug 4 ; 23(15):3154-63.
この記事をPubMed上で見るPubMedで表示
この記事をGoogle翻訳上で見る Google翻訳で開く

UPR2169 CNRS, Genetic Instability and Cancer, Institut Gustave Roussy, Pavillon de Recherche, Rue Camille Desmoulins, Villejuif, France. pichierri70@virgilio.it

スターを付ける スターを付ける     (95view , 0users)

Full Text Sources

Miscellaneous

Research Materials

Fanconi anaemia (FA) and Bloom syndrome (BS) are autosomal recessive diseases characterised by chromosome fragility and cancer proneness. Here, we report that BLM and the FA pathway are activated in response to both crosslinked DNA and replication fork stall. We provide evidence that BLM and FANCD2 colocalise and co-immunoprecipitate following treatment with either DNA crosslinkers or agents inducing replication arrest. We also find that the FA core complex is necessary for BLM phosphorylation and assembly in nuclear foci in response to crosslinked DNA. Moreover, we show that knock-down of the MRE11 complex, whose function is also under the control of the FA core complex, enhances cellular and chromosomal sensitivity to DNA interstrand crosslinks in BS cells. These findings suggest the existence of a functional link between BLM and the FA pathway and that BLM and the MRE11 complex are in two separated branches of a pathway resulting in S-phase checkpoint activation, chromosome integrity and cell survival in response to crosslinked DNA.
PMID: 15257300 [PubMed - indexed for MEDLINE]
印刷用ページを開く Endnote用テキストダウンロード