Effects of Base Sequence Context on Translesion Synthesis Past a Bulky (+)-trans-anti-B[a]P-N2-dG Lesion Catalyzed by the Y-family Polymerase pol κ†

Biochemistry ◽  
2003 ◽  
Vol 42 (8) ◽  
pp. 2456-2466 ◽  
Author(s):  
Xuanwei Huang ◽  
Alexander Kolbanovskiy ◽  
Xiaohua Wu ◽  
Yanbin Zhang ◽  
Zhigang Wang ◽  
...  
Keyword(s):  
Translesion Synthesis ◽  
Base Sequence ◽  
Sequence Context ◽  
Y Family

scholarly journals Polη, a Y-family translesion synthesis polymerase, promotes cellular tolerance of Myc-induced replication stress

2018 ◽  
Vol 131 (12) ◽  
pp. jcs212183 ◽  
Author(s):  
Kiminori Kurashima ◽  
Takayuki Sekimoto ◽  
Tsukasa Oda ◽  
Tsuyoshi Kawabata ◽  
Fumio Hanaoka ◽  
...  
Keyword(s):  
Translesion Synthesis ◽  
Replication Stress ◽  
Cellular Tolerance ◽  
Y Family

scholarly journals Y-family DNA polymerase-independent gap-filling translesion synthesis across aristolochic acid-derived adenine adducts in mouse cells

DNA Repair ◽  
2016 ◽  
Vol 46 ◽  
pp. 55-60 ◽  
Author(s):  
Keiji Hashimoto ◽  
Radha Bonala ◽  
Francis Johnson ◽  
Arthur P. Grollman ◽  
Masaaki Moriya
Keyword(s):  
Dna Polymerase ◽  
Aristolochic Acid ◽  
Translesion Synthesis ◽  
Gap Filling ◽  
Mouse Cells ◽  
Adenine Adducts ◽  
Y Family

scholarly journals Distant Neighbor Base Sequence Context Effects in Human Nucleotide Excision Repair of a Benzo[a]pyrene-derived DNA Lesion

2010 ◽  
Vol 399 (3) ◽  
pp. 397-409 ◽  
Author(s):  
Yuqin Cai ◽  
Konstantin Kropachev ◽  
Rong Xu ◽  
Yijin Tang ◽  
Marina Kolbanovskii ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Context Effects ◽  
Excision Repair ◽  
Base Sequence ◽  
Sequence Context ◽  
Dna Lesion ◽  
Nucleotide Excision ◽  
Distant Neighbor

Role of Base Sequence Context in Conformational Equilibria and Nucleotide Excision Repair of Benzo[a]pyrene Diol Epoxide−Adenine Adducts†

Biochemistry ◽  
2003 ◽  
Vol 42 (8) ◽  
pp. 2339-2354 ◽  
Author(s):  
Shixiang Yan ◽  
Min Wu ◽  
Tonko Buterin ◽  
Hanspeter Naegeli ◽  
Nicholas E. Geacintov ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Base Sequence ◽  
Sequence Context ◽  
Diol Epoxide ◽  
Nucleotide Excision ◽  
Conformational Equilibria ◽  
Adenine Adducts

scholarly journals Translesion Synthesis across Abasic Lesions by Human B-Family and Y-Family DNA Polymerases α, δ, η, ι, κ, and REV1

2010 ◽  
Vol 404 (1) ◽  
pp. 34-44 ◽  
Author(s):  
Jeong-Yun Choi ◽  
Seonhee Lim ◽  
Eun-Jin Kim ◽  
Ara Jo ◽  
F. Peter Guengerich
Keyword(s):  
Dna Polymerases ◽  
Translesion Synthesis ◽  
Y Family

scholarly journals Implications of inhibition of Rev1 interaction with Y family DNA polymerases for cisplatin chemotherapy

2021 ◽  
Author(s):  
Jung-Hoon Yoon ◽  
Robert E. Johnson ◽  
Louise Prakash ◽  
Satya Prakash
Keyword(s):  
Adverse Effects ◽  
Cancer Cells ◽  
Dna Polymerases ◽  
Translesion Synthesis ◽  
Dna Adduct ◽  
Secondary Malignancies ◽  
Normal Cells ◽  
Cross Links ◽  
Y Family

Chemotherapy with cisplatin becomes limiting due to toxicity and secondary malignancies. In principle, therapeutics could be improved by targeting translesion synthesis (TLS) polymerases (Pols) that promote replication through intrastrand cross-links, the major cisplatin-induced DNA adduct. However, to specifically target malignancies with minimal adverse effects on normal cells, a good understanding of TLS mechanisms in normal versus cancer cells is paramount. We show that in normal cells, TLS through cisplatin intrastrand cross-links is promoted by Polη- or Polι-dependent pathways, both of which require Rev1 as a scaffolding component. In contrast, cancer cells require Rev1-Polζ. Our findings that a recently identified Rev1 inhibitor, JH-RE-06, purported to specifically disrupt Rev1 interaction with Polζ to block TLS through cisplatin adducts in cancer cells, abrogates Rev1's ability to function with Y family Pols as well, implying that by inactivating Rev1-dependent TLS in normal cells, this inhibitor will exacerbate the toxicity and tumorigenicity of chemotherapeutics with cisplatin.

scholarly journals Mechanism of Translesion Synthesis Past an Equine Estrogen-DNA Adduct by Y-Family DNA Polymerases

2007 ◽  
Vol 371 (5) ◽  
pp. 1151-1162 ◽  
Author(s):  
Manabu Yasui ◽  
Naomi Suzuki ◽  
Xiaoping Liu ◽  
Yoshinori Okamoto ◽  
Sung Yeon Kim ◽  
...  
Keyword(s):  
Dna Polymerases ◽  
Translesion Synthesis ◽  
Dna Adduct ◽  
Y Family

scholarly journals ATR-mediated phosphorylation of DNA polymerase η is needed for efficient recovery from UV damage

2011 ◽  
Vol 192 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Thomas Göhler ◽  
Simone Sabbioneda ◽  
Catherine M. Green ◽  
Alan R. Lehmann
Keyword(s):  
Dna Damage ◽  
Dna Polymerase ◽  
Mammalian Cells ◽  
Translesion Synthesis ◽  
Physical Interaction ◽  
Uv Damage ◽  
Checkpoint Response ◽  
Ubiquitin Binding Domain ◽  
Efficient Recovery ◽  
Y Family

DNA polymerase η (polη) belongs to the Y-family of DNA polymerases and facilitates translesion synthesis past UV damage. We show that, after UV irradiation, polη becomes phosphorylated at Ser601 by the ataxia-telangiectasia mutated and Rad3-related (ATR) kinase. DNA damage–induced phosphorylation of polη depends on its physical interaction with Rad18 but is independent of PCNA monoubiquitination. It requires the ubiquitin-binding domain of polη but not its PCNA-interacting motif. ATR-dependent phosphorylation of polη is necessary to restore normal survival and postreplication repair after ultraviolet irradiation in xeroderma pigmentosum variant fibroblasts, and is involved in the checkpoint response to UV damage. Taken together, our results provide evidence for a link between DNA damage–induced checkpoint activation and translesion synthesis in mammalian cells.

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