Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase

Research output: Contribution to journal › Journal article › Research › peer-review

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Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase. / Duan, Shunlei; Han, Xuerui; Akbari, Mansour; Croteau, Deborah L; Rasmussen, Lene Juel; Bohr, Vilhelm.

In: Nucleic Acids Research, Vol. 48, No. 12, 2020, p. 6530–6546.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Duan, S, Han, X, Akbari, M, Croteau, DL, Rasmussen, LJ & Bohr, V 2020, 'Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase', Nucleic Acids Research, vol. 48, no. 12, pp. 6530–6546. https://doi.org/10.1093/nar/gkaa392

APA

Duan, S., Han, X., Akbari, M., Croteau, D. L., Rasmussen, L. J., & Bohr, V. (2020). Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase. Nucleic Acids Research, 48(12), 6530–6546. https://doi.org/10.1093/nar/gkaa392

Vancouver

Duan S, Han X, Akbari M, Croteau DL, Rasmussen LJ, Bohr V. Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase. Nucleic Acids Research. 2020;48(12):6530–6546. https://doi.org/10.1093/nar/gkaa392

Author

Duan, Shunlei ; Han, Xuerui ; Akbari, Mansour ; Croteau, Deborah L ; Rasmussen, Lene Juel ; Bohr, Vilhelm. / Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase. In: Nucleic Acids Research. 2020 ; Vol. 48, No. 12. pp. 6530–6546.

Bibtex

@article{d6133855330f410c965680d05e451ed1,
title = "Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase",
abstract = "OGG1 initiated base excision repair (BER) is the major pathway for repair of oxidative DNA base damage 8-oxoguanine (8-oxoG). Here, we report that RECQL4 DNA helicase, deficient in the cancer-prone and premature aging Rothmund-Thomson syndrome, physically and functionally interacts with OGG1. RECQL4 promotes catalytic activity of OGG1 and RECQL4 deficiency results in defective 8-oxoG repair and increased genomic 8-oxoG. Furthermore, we show that acute oxidative stress leads to increased RECQL4 acetylation and its interaction with OGG1. The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state. Collectively, we find that RECQL4 is involved in 8-oxoG repair through interaction with OGG1, and that SIRT1 indirectly modulates BER of 8-oxoG by controlling RECQL4–OGG1 interaction",
author = "Shunlei Duan and Xuerui Han and Mansour Akbari and Croteau, {Deborah L} and Rasmussen, {Lene Juel} and Vilhelm Bohr",
year = "2020",
doi = "10.1093/nar/gkaa392",
language = "English",
volume = "48",
pages = "6530–6546",
journal = "Nucleic Acids Research",
issn = "0305-1048",
publisher = "Oxford University Press",
number = "12",

}

RIS

TY - JOUR

T1 - Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase

AU - Duan, Shunlei

AU - Han, Xuerui

AU - Akbari, Mansour

AU - Croteau, Deborah L

AU - Rasmussen, Lene Juel

AU - Bohr, Vilhelm

PY - 2020

Y1 - 2020

N2 - OGG1 initiated base excision repair (BER) is the major pathway for repair of oxidative DNA base damage 8-oxoguanine (8-oxoG). Here, we report that RECQL4 DNA helicase, deficient in the cancer-prone and premature aging Rothmund-Thomson syndrome, physically and functionally interacts with OGG1. RECQL4 promotes catalytic activity of OGG1 and RECQL4 deficiency results in defective 8-oxoG repair and increased genomic 8-oxoG. Furthermore, we show that acute oxidative stress leads to increased RECQL4 acetylation and its interaction with OGG1. The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state. Collectively, we find that RECQL4 is involved in 8-oxoG repair through interaction with OGG1, and that SIRT1 indirectly modulates BER of 8-oxoG by controlling RECQL4–OGG1 interaction

AB - OGG1 initiated base excision repair (BER) is the major pathway for repair of oxidative DNA base damage 8-oxoguanine (8-oxoG). Here, we report that RECQL4 DNA helicase, deficient in the cancer-prone and premature aging Rothmund-Thomson syndrome, physically and functionally interacts with OGG1. RECQL4 promotes catalytic activity of OGG1 and RECQL4 deficiency results in defective 8-oxoG repair and increased genomic 8-oxoG. Furthermore, we show that acute oxidative stress leads to increased RECQL4 acetylation and its interaction with OGG1. The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state. Collectively, we find that RECQL4 is involved in 8-oxoG repair through interaction with OGG1, and that SIRT1 indirectly modulates BER of 8-oxoG by controlling RECQL4–OGG1 interaction

U2 - 10.1093/nar/gkaa392

DO - 10.1093/nar/gkaa392

M3 - Journal article

C2 - 32432680

VL - 48

SP - 6530

EP - 6546

JO - Nucleic Acids Research

JF - Nucleic Acids Research

SN - 0305-1048

IS - 12

ER -

ID: 245004891