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Involvement of SPRTN in DNA protein cross-link damage repair

https://repo.qst.go.jp/records/80335
https://repo.qst.go.jp/records/80335
6b910066-5640-4fbb-8b10-d97c7bef712f
Item type 会議発表用資料 / Presentation(1)
公開日 2020-08-18
タイトル
タイトル Involvement of SPRTN in DNA protein cross-link damage repair
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference object
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Nakano, Toshiaki

× Nakano, Toshiaki

WEKO 882352

Nakano, Toshiaki

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Sasanum, Hiroyuki

× Sasanum, Hiroyuki

WEKO 882353

Sasanum, Hiroyuki

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Tuda, Masataka

× Tuda, Masataka

WEKO 882354

Tuda, Masataka

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Hirota, Kouji

× Hirota, Kouji

WEKO 882355

Hirota, Kouji

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Shikazono, Naoya

× Shikazono, Naoya

WEKO 882356

Shikazono, Naoya

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Kawanishi, Masanobu

× Kawanishi, Masanobu

WEKO 882357

Kawanishi, Masanobu

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Takeda, Shunichi

× Takeda, Shunichi

WEKO 882358

Takeda, Shunichi

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Ide, Hiroshi

× Ide, Hiroshi

WEKO 882359

Ide, Hiroshi

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Tano, Keizo

× Tano, Keizo

WEKO 882360

Tano, Keizo

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Nakano, Toshiaki

× Nakano, Toshiaki

WEKO 882361

en Nakano, Toshiaki

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Shikazono, Naoya

× Shikazono, Naoya

WEKO 882362

en Shikazono, Naoya

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抄録
内容記述タイプ Abstract
内容記述 DNA-protein cross links (DPCs) are caused by covalently linking DNA and DNA-associated proteins and by intermediates of DNA-metabolizing enzymes. Current studies showed that SPRTN, metalloprotease, is a critical factor in proteolytic cleavage of DPCs. However, it has not been clarified which proteins are targets for SPRTN. In this study, we examined the contribution of SPRTN to cleave DPCs using a reverse genetic strategy with human lymphocytes, TK6. Cells deficient in SPRTN were not sensitive to formaldehyde (FA) producing DPCs with various proteins. In contrast, these cells showed hyper-sensitive to aza-deoxycytidine (azadC) which specifically trapped methyltransferase (Dnmt1) to DNA (Dnmt1-DPCs). AzadC treatment resulted in the accumulation of Dnmt1-DPCs in purified genomic DNA. The rate of removal of Dnmt1-DPCs was slower in sprtn-deficient cells than in wild type cells. Our data suggest that SPRTN plays critical role in the resolution of Dnmt1-DPCs in human cells.
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 第43回 日本分子生物学会
発表年月日
日付 2020-12-02
日付タイプ Issued
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