Posttranslational modification of mammalian AP endonuclease (APE1)

被引：44

作者：

Busso, Carlos S. ^{[1
,2
]}

Lake, Michael W. ^{[1
,2
]}

Izumi, Tadahide ^{[1
,2
]}

机构：

[1] Louisiana State Univ Hlth Sci Ctr, Dept Otorhinolaryngol, New Orleans, LA 70112 USA

[2] Louisiana State Univ Hlth Sci Ctr, Stanley S Scott Canc Ctr, New Orleans, LA 70112 USA

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 2010年 / 67卷 / 21期

关键词：

DNA base excision repair; APE1; Phosphorylation; Acetylation; Ubiquitination; OXIDATIVE DNA-DAMAGE; HUMAN APURINIC ENDONUCLEASE; UBIQUITIN-PROTEIN LIGASE; SINGLE-STRAND BREAKS; ABASIC SITE REPAIR; APURINIC/APYRIMIDINIC ENDONUCLEASE-1; POLY(ADP-RIBOSE) POLYMERASE; P53; APE1/REF-1; REDOX;

D O I：

10.1007/s00018-010-0487-3

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

A key issue in studying mammalian DNA base excision repair is how its component proteins respond to a plethora of cell-signaling mediators invoked by DNA damage and stress-inducing agents such as reactive oxygen species, and how the actions of individual BER proteins are attributed to cell survival or apoptotic/necrotic death. This article reviews the past and recent progress on posttranslational modification (PTM) of mammalian apurinic/apyrimidinic (AP) endonuclease 1 (APE1).

引用

页码：3609 / 3620

页数：12

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