Alternative nucleotide incision repair pathway for oxidative DNA damage

Ischenko, Alexander A.; Saparbaev, Murat

doi:10.1038/415183a

Cited by 277 publications

(198 citation statements)

References 29 publications

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“…In other words, for specific types of oxidative damage, APE1 has the ability to cleave the damaged DNA strand in a glycosylase-independent manner. This novel function of APE1 was the driving force behind the development of the alternative BER pathway called nucleotide incision repair (NIR) [41]. Although kinetic data suggest that 5-hydroxy-2'-deoxycytidine (5OH-C) residues are inefficiently repaired by DNA glycosylases NTH1 and NEIL1 coupled with either APE1 3'phosphodiesterase or 3'phosphotase activity, Daviet et.…”

Section: Direct Ape1-mediated Nucleotide Incision As An Initiator Of Bermentioning

confidence: 99%

A unified view of base excision repair: Lesion-dependent protein complexes regulated by post-translational modification

Almeida¹,

Sobol²

2007

DNA Repair

379

374

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Base excision repair (BER) proteins act upon a significantly broad spectrum of DNA lesions that result from endogenous and exogenous sources. Multiple sub-pathways of BER (short-path or longpatch) and newly designated DNA repair pathways (e.g., SSBR and NIR) that utilize BER proteins complicate any comprehensive understanding of BER and its role in genome maintenance, chemotherapeutic response, neurodegeneration, cancer or aging. Herein, we propose a unified model of BER, comprised of three functional processes: Lesion Recognition/Strand Scission, Gap Tailoring and DNA Synthesis/Ligation, each represented by one or more multiprotein complexes and coordinated via the XRCC1/DNA Ligase III and PARP1 scaffold proteins. BER therefore may be represented by a series of repair complexes that assemble at the site of the DNA lesion and mediates repair in a coordinated fashion involving protein-protein interactions that dictate subsequent steps or sub-pathway choice. Complex formation is influenced by post-translational protein modifications that arise from the cellular state or the DNA damage response, providing an increase in specificity and efficiency to the BER pathway. In this review, we have summarized the reported BER proteinprotein interactions and protein post-translational modifications and discuss the impact on DNA repair capacity and complex formation.

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Section: Direct Ape1-mediated Nucleotide Incision As An Initiator Of Bermentioning

confidence: 99%

A unified view of base excision repair: Lesion-dependent protein complexes regulated by post-translational modification

Almeida¹,

Sobol²

2007

DNA Repair

379

374

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“…However, a direct incision activity immediately 5 0 to oxidized bases was identified in the Endo IV-type AP endonuclease (encoded by the nfo gene) from E. coli as well as a similar activity in budding yeast and human cell extracts (Ischenko and Saparbaev 2002). This incision leaves 3 0 -hydroxyl termini for further DNA synthesis and repair, which was designated as nucleotide incision repair (NIR) by the authors.…”

Section: Nir Aer and Ssb Repairmentioning

confidence: 99%

Alternative Excision Repair Pathways

Yasui

2013

Cold Spring Harbor Perspectives in Biology

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Alternative excision repair (AER) is a category of excision repair initiated by a single nick, made by an endonuclease, near the site of DNA damage, and followed by excision of the damaged DNA, repair synthesis, and ligation. The ultraviolet (UV) damage endonuclease in fungi and bacteria introduces a nick immediately 5 0 to various types of UV damage and initiates its excision repair that is independent of nucleotide excision repair (NER). Endo IVtype apurinic/apyrimidinic (AP) endonucleases from Escherichia coli and yeast and human Exo III-type AP endonuclease APEX1 introduce a nick directly and immediately 5 0 to various types of oxidative base damage besides the AP site, initiating excision repair. Another endonuclease, endonuclease V from bacteria to humans, binds deaminated bases and cleaves the phosphodiester bond located 1 nucleotide 3 0 of the base, leading to excision repair. A singlestrand break in DNA is one of the most frequent types of DNA damage within cells and is repaired efficiently. AER makes use of such repair capability of single-strand breaks, removes DNA damage, and has an important role in complementing BER and NER.N ER and base excision repair (BER) are the major excision repair pathways present in almost all organisms. In NER, dual incisions are introduced, the damaged DNA between the incised sites is then removed, and DNA synthesis fills the single-stranded gap, followed by ligation. In BER, an AP site, formed by depurination or created by a base damage-specific DNA glycosylase, is recognized by an AP endonuclease that introduces a nick immediately 5 0 to the AP site, followed by repair synthesis, removal of the AP site, and final ligation. Besides these two fundamental excision repair systems, investigators have found another category of excision repair-AER-an example of which is the excision repair of UV damage, initiated by an endonuclease called UV damage endonuclease (UVDE).UVDE introduces a single nick immediately 5 0 to various types of UV lesions as well as other types of base damage, and this nick leads to the removal of the lesions by an AER process designated as UVDE-mediated excision repair (UVER or UVDR). Genetic analysis in Schizosaccharomyces pombe indicates that UVER provides cells with an extremely rapid removal of UV lesions, which is important for cells exposed to UV in their growing phase.Endo IV-type AP endonucleases from Escherichia coli and budding yeast and the Exo III -type human AP endonuclease APEX1 are able to introduce a nick at various types of oxidative base damage and initiate a form of excision repair that has been designated as nucleotide incision repair (NIR). Endonuclease V

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“…4) using a similar mode of action. (101,102) It therefore appears that this type of repair mechanism is implicated in removal of various classes of DNA damage.…”

Section: Repair Of Six-membered Propano-g Derivatives and M 1 G By Thmentioning

confidence: 99%

Repair of exocyclic DNA adducts: rings of complexity

Hang

2004

BioEssays

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SummaryExocyclic DNA adducts are mutagenic lesions that can be formed by both exogenous and endogenous mutagens/ carcinogens. These adducts are structurally analogs but can differ in certain features such as ring size, conjugation, planarity and substitution. Although the information on the biological role of the repair activities for these adducts is largely unknown, considerable progress has been made on their reaction mechanisms, substrate specificities and kinetic properties that are affected by adduct structures. At least four different mechanisms appear to have evolved for the removal of specific exocyclic adducts. These include base excision repair, nucleotide excision repair, mismatch repair, and AP endonuclease-mediated repair. This overview highlights the recent progress in such areas with emphasis on structure-activity relationships. It is also apparent that more information is needed for a better understanding of the biological and structural implications of exocyclic adducts and their repair.

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Alternative nucleotide incision repair pathway for oxidative DNA damage

Cited by 277 publications

References 29 publications

A unified view of base excision repair: Lesion-dependent protein complexes regulated by post-translational modification

A unified view of base excision repair: Lesion-dependent protein complexes regulated by post-translational modification

Alternative Excision Repair Pathways

Repair of exocyclic DNA adducts: rings of complexity

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