ログイン
言語:

WEKO3

  • トップ
  • ランキング
To
lat lon distance
To

Field does not validate



インデックスリンク

インデックスツリー

メールアドレスを入力してください。

WEKO

One fine body…

WEKO

One fine body…

アイテム

  1. その他誌上発表

Radiaiton-induced delayed genome instability and hypermutation in mammalian cells

https://repo.qst.go.jp/records/58252
https://repo.qst.go.jp/records/58252
29263d14-e8b2-483d-b830-fbd62b0d1953
Item type 一般雑誌記事 / Article(1)
公開日 2013-06-07
タイトル
タイトル Radiaiton-induced delayed genome instability and hypermutation in mammalian cells
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_6501
資源タイプ article
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 Allen, Christopher

× Allen, Christopher

WEKO 583891

Allen, Christopher

Search repository
Fujimori, Akira

× Fujimori, Akira

WEKO 583892

Fujimori, Akira

Search repository
Okayasu, Ryuichi

× Okayasu, Ryuichi

WEKO 583893

Okayasu, Ryuichi

Search repository
Nickoloff, Jac

× Nickoloff, Jac

WEKO 583894

Nickoloff, Jac

Search repository
アレン クリストファー

× アレン クリストファー

WEKO 583895

en アレン クリストファー

Search repository
藤森 亮

× 藤森 亮

WEKO 583896

en 藤森 亮

Search repository
岡安 隆一

× 岡安 隆一

WEKO 583897

en 岡安 隆一

Search repository
抄録
内容記述タイプ Abstract
内容記述 Genome instability is a hallmark of cancer cells. Inherited cancer predisposition syndromes typically show defects in DNA repair or DNA damage checkpoint systems, collectively called the DNA damage response (DDR). Several mutations in key genes are required to convert a normal cell to a cancer cell, suggesting that an early step in carcinogenesis is the acquisition of a 'genome instability' (mutator) phenotype. DDR proteins suppress cancer by preventing spontaneous damage from causing excessive genome instability, and thus, normal cells display very low mutation rates and stable genomes. Genotoxins such as DNA-reactive chemicals and radiation cause DNA damage that results in small- and large-scale genetic change (mutations). Recently it has become clear that radiation, including ionizing radiation (IR) such X-rays and charged particles (heavy ion radiation), as well as nonionizing radiation (UV light) induce genome instability many cell generations after the exposure. These delayed effects are seen after high (1-10 Gy) and very low (0.01-0.1 Gy) IR doses, and include hypermutation, hyper-homologous recombination, chromosome instability, and reduced clonogenic survival (delayed death). Similar to immediate effects of radiation, delayed effects show adaptive responses. Here we focus on potential mechanisms that underlie radiation-induced delayed genome instabilities, and discuss the risks of genome destabilizing effects of occupational and accidental radiation exposures, and clinical exposures associated with radiation therapy and diagnostic imaging procedures.
書誌情報 Stress-Induced Mutagenesis

p. 183-198, 発行日 2013
出版者
出版者 Springer
ISBN
識別子タイプ ISBN
関連識別子 978-1-4614-6279
戻る
0
views
See details
Views

Versions

Ver.1 2023-05-15 22:18:01.127280
Show All versions

Share

Mendeley Twitter Facebook Print Addthis

Cite as

エクスポート

OAI-PMH
  • OAI-PMH JPCOAR 2.0
  • OAI-PMH JPCOAR 1.0
  • OAI-PMH DublinCore
  • OAI-PMH DDI
Other Formats
  • JSON
  • BIBTEX

Confirm


Powered by WEKO3


Powered by WEKO3