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Orchestration of base excision repair by controlling the rates of enzymatic activities.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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Orchestration of base excision repair by controlling the rates of enzymatic activities. / Allinson, Sarah L.; Sleeth, Kate M.; Matthewman, Gemma E. et al.
In: DNA Repair, Vol. 3, No. 1, 01.2004, p. 23-31.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Allinson, SL, Sleeth, KM, Matthewman, GE & Dianov, GL 2004, 'Orchestration of base excision repair by controlling the rates of enzymatic activities.', DNA Repair, vol. 3, no. 1, pp. 23-31. https://doi.org/10.1016/j.dnarep.2003.09.002

APA

Allinson, S. L., Sleeth, K. M., Matthewman, G. E., & Dianov, G. L. (2004). Orchestration of base excision repair by controlling the rates of enzymatic activities. DNA Repair, 3(1), 23-31. https://doi.org/10.1016/j.dnarep.2003.09.002

Vancouver

Allinson SL, Sleeth KM, Matthewman GE, Dianov GL. Orchestration of base excision repair by controlling the rates of enzymatic activities. DNA Repair. 2004 Jan;3(1):23-31. doi: 10.1016/j.dnarep.2003.09.002

Author

Allinson, Sarah L. ; Sleeth, Kate M. ; Matthewman, Gemma E. et al. / Orchestration of base excision repair by controlling the rates of enzymatic activities. In: DNA Repair. 2004 ; Vol. 3, No. 1. pp. 23-31.

Bibtex

@article{2ef6a09962d04918be0183513167b4aa,
title = "Orchestration of base excision repair by controlling the rates of enzymatic activities.",
abstract = "Base excision repair (BER) is one of the major pathways for repair of simple DNA base lesions and is carried out through a series of coordinated reactions relying on several different enzymatic activities and accessory proteins. Imbalance of BER activities has been reported to be linked to genetic instability and cancer. To experimentally address the mechanisms orchestrating BER, we monitored both the overall rate and the rate-limiting steps in the repair in cell-free extracts of five different endogenously occurring DNA lesions (abasic site, uracil, 8-oxoguanine, hypoxanthine and 5,6-dihydrouracil) and the effect of addition of rate-limiting BER components on the rate and co-ordination of BER reactions. We find that several mechanisms including regulation of DNA glycosylase turnover and involvement of poly(ADP-ribose) polymerase participate in synchronization of the repair events. We also find that repair of different DNA lesions involves different mechanisms for optimizing repair rates without accumulation of intermediates. Repair of some lesions such as 8-oxoguanine is regulated by glycosylase turnover and progress without substantial accumulation of repair intermediates. However, during repair of the apurinic/apyrimidinic (AP) sites or 5,6-dihydrouracil, poly(ADP-ribose) polymerase plays an important role in the coordination of the rates of repair reactions.",
keywords = "Base lesions, Base excision repair, Human cell extracts, Pol β, AP endonuclease, PARP",
author = "Allinson, {Sarah L.} and Sleeth, {Kate M.} and Matthewman, {Gemma E.} and Dianov, {Grigory L.}",
year = "2004",
month = jan,
doi = "10.1016/j.dnarep.2003.09.002",
language = "English",
volume = "3",
pages = "23--31",
journal = "DNA Repair",
issn = "1568-7864",
publisher = "Elsevier",
number = "1",

}

RIS

TY - JOUR

T1 - Orchestration of base excision repair by controlling the rates of enzymatic activities.

AU - Allinson, Sarah L.

AU - Sleeth, Kate M.

AU - Matthewman, Gemma E.

AU - Dianov, Grigory L.

PY - 2004/1

Y1 - 2004/1

N2 - Base excision repair (BER) is one of the major pathways for repair of simple DNA base lesions and is carried out through a series of coordinated reactions relying on several different enzymatic activities and accessory proteins. Imbalance of BER activities has been reported to be linked to genetic instability and cancer. To experimentally address the mechanisms orchestrating BER, we monitored both the overall rate and the rate-limiting steps in the repair in cell-free extracts of five different endogenously occurring DNA lesions (abasic site, uracil, 8-oxoguanine, hypoxanthine and 5,6-dihydrouracil) and the effect of addition of rate-limiting BER components on the rate and co-ordination of BER reactions. We find that several mechanisms including regulation of DNA glycosylase turnover and involvement of poly(ADP-ribose) polymerase participate in synchronization of the repair events. We also find that repair of different DNA lesions involves different mechanisms for optimizing repair rates without accumulation of intermediates. Repair of some lesions such as 8-oxoguanine is regulated by glycosylase turnover and progress without substantial accumulation of repair intermediates. However, during repair of the apurinic/apyrimidinic (AP) sites or 5,6-dihydrouracil, poly(ADP-ribose) polymerase plays an important role in the coordination of the rates of repair reactions.

AB - Base excision repair (BER) is one of the major pathways for repair of simple DNA base lesions and is carried out through a series of coordinated reactions relying on several different enzymatic activities and accessory proteins. Imbalance of BER activities has been reported to be linked to genetic instability and cancer. To experimentally address the mechanisms orchestrating BER, we monitored both the overall rate and the rate-limiting steps in the repair in cell-free extracts of five different endogenously occurring DNA lesions (abasic site, uracil, 8-oxoguanine, hypoxanthine and 5,6-dihydrouracil) and the effect of addition of rate-limiting BER components on the rate and co-ordination of BER reactions. We find that several mechanisms including regulation of DNA glycosylase turnover and involvement of poly(ADP-ribose) polymerase participate in synchronization of the repair events. We also find that repair of different DNA lesions involves different mechanisms for optimizing repair rates without accumulation of intermediates. Repair of some lesions such as 8-oxoguanine is regulated by glycosylase turnover and progress without substantial accumulation of repair intermediates. However, during repair of the apurinic/apyrimidinic (AP) sites or 5,6-dihydrouracil, poly(ADP-ribose) polymerase plays an important role in the coordination of the rates of repair reactions.

KW - Base lesions

KW - Base excision repair

KW - Human cell extracts

KW - Pol β

KW - AP endonuclease

KW - PARP

U2 - 10.1016/j.dnarep.2003.09.002

DO - 10.1016/j.dnarep.2003.09.002

M3 - Journal article

VL - 3

SP - 23

EP - 31

JO - DNA Repair

JF - DNA Repair

SN - 1568-7864

IS - 1

ER -