Preferential binding of human XPA to the mitomycin C-DNA interstrand crosslink and modulation by arsenic and cadmium

Mustra, David; Warren, Amy J.; Wilcox, Dean E.; Hamilton, Joshua W.

doi:10.1016/j.cbi.2007.04.004

Cited by 21 publications

(15 citation statements)

References 27 publications

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“…Besides effects on XPC and XPCdependent processes, reduced DNA damage recognition and therefore reduced incision frequencies may additionally result from interaction of the arsenicals with XPA function. Subcellular studies previously investigated the impact of arsenite on XPA binding to a UVC- [57] or MMC-damaged [58] oligonucleotide; they demonstrated no decrease of XPA binding or XPA binding inhibition only at high micromolar to millimolar concentrations of arsenite. Consistently, it has recently been shown that in case of a synthesized peptide representing the zinc finger structure of the human XPA (XPAzf), the zinc containing peptide was totally resistant to equimolar arsenite concentrations.…”

Section: Discussionmentioning

confidence: 98%

Impact of arsenic on nucleotide excision repair: XPC function, protein level, and gene expression

Nollen

Ebert

Moser

et al. 2009

Molecular Nutrition Food Res

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The ubiquitous occurrence of the human carcinogen arsenic results in multiple exposure possibilities to humans. The human diet, especially drinking water, is the primary source of inorganic arsenic intake in the general population. The ingested arsenic is metabolized to methylated derivatives; some of these metabolites are today considered to be more toxic than the inorganic species. Various modes of action have been proposed to contribute to arsenic carcinogenicity; inhibition of nucleotide excision repair (NER), removing DNA helix distorting DNA adducts induced by environmental mutagens, is likely to be of primary importance. Here, we report that arsenite and its metabolite monomethylarsonous acid (MMA(III)) strongly decreased expression and protein level of Xeroderma pigmentosum complementation group C (XPC), which is believed to be the principle initiator of global genome NER. This led to diminished association of XPC to sites of local UVC damage, resulting in decreased recruitment of further NER proteins. Additionally Xeroderma pigmentosum complementation group E protein (XPE) expression was reduced, which encodes for another important NER protein and similarly to XPC is regulated by the activity of the transcription factor p53. In summary, our data demonstrate that in human skin fibroblasts arsenite and even more pronounced MMA(III) interact with XPC expression, resulting in decreased XPC protein level and diminished assembly of the NER machinery.

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Section: Discussionmentioning

confidence: 98%

Impact of arsenic on nucleotide excision repair: XPC function, protein level, and gene expression

Nollen

Ebert

Moser

et al. 2009

Molecular Nutrition Food Res

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“…Because the precise mechanistic details of ICL repair are unknown, cell-free extracts have been used to examine how ICLs are processed. Some studies have been carried out using purified enzymes that have been implicated in ICL recognition and incision (Kuraoka et al 2000; Mustra et al 2001; Mustra et al 2007; Fisher et al 2008; Zhao et al 2009). However, reconstitution of the initial steps of recognition and unhooking of a cross-link from quiescent DNA has yet to be realized with recombinant proteins.…”

Section: Icl Repair In Quiescent Dnamentioning

confidence: 99%

“…Studies using purified proteins have examined the ability of proteins implicated in ICL repair to specifically recognize ICL substrates (Kuraoka et al 2000; Mustra et al 2001; Mustra et al 2007; Fisher et al 2008; Zhao et al 2009). Other studies have focused on the ability of the XPF-ERCC1 nuclease to cleave cross-linked substrates because of its apparent special role in ICL repair (Kuraoka et al 2000; Fisher et al 2008).…”

Section: Icl Repair In Quiescent Dnamentioning

confidence: 99%

“…The damage recognition components of the NER pathway are XPC-hHR23B and XPA-RPA. XPA has been shown to have some level of specificity towards a mitomycin C cross-linked substrate and undergo a conformational change upon binding to the lesion (Mustra et al 2001; Mustra et al 2007). Both XPC-hHR23B and XPA-RPA were shown to bind selectively to an ICL that was placed in a triplex-forming oligonucleotide (TFO) (Thoma et al 2005).…”

Section: Icl Repair In Quiescent Dnamentioning

confidence: 99%

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Initiation of DNA interstrand cross‐link repair in mammalian cells

Hlavin

Smeaton

Miller

2010

Environ and Mol Mutagen

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Interstrand cross-links (ICLs) are among the most cytotoxic DNA lesions to cells because they prevent the two DNA strands from separating, thereby precluding replication and transcription. Even though chemotherapeutic cross-linking agents are well established in clinical use, and numerous repair proteins have been implicated in the initial events of mammalian ICL repair, the precise mechanistic details of these events remain to be elucidated. This review will summarize our current understanding of how ICL repair is initiated with an emphasis on the context (replicating, transcribed or quiescent DNA) in which the ICL is recognized, and how the chemical and physical properties of ICLs influence repair. Although most studies have focused on replication-dependent repair because of the relation to highly replicative tumor cells, replicationindependent ICL repair is likely to be important in the circumvention of cross-link cytotoxicity in non-dividing, terminally differentiated cells that may be challenged with exogenous or endogenous sources of ICLs. Consequently, the ICL repair pathway that should be considered 'dominant' appears to depend on the cell type and the DNA context in which the ICL is encountered. The ability to define and inhibit distinct pathways of ICL repair in different cell cycle phases may help in developing methods that increase cytotoxicity to cancer cells while reducing side-effects in non-dividing normal cells. This may also lead to a better understanding of pathways that protect against malignancy and aging.

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“…Proteins from both the NER and MMR mechanisms have been implicated in the repair of and response to ICLs in mammalian cells (Barre et al 1999a; Datta et al 2001; Faruqi et al 2000; McHugh et al 2001; Mustra et al2007; Sarkar et al 2006; Vasquez et al 2002; Wu et al 2005; Wu and Vasquez 2008; Zhang et al 2002). It has been proposed that there is an S-phase and recombination-dependent error-free pathway and a recombination-independent error-generating pathway of ICL repair in human cells predominantly in G 0 or G 1 -phase cells (McHugh and Sarkar 2006; Noll et al 2006).…”

Section: Repair Of Psoralen Iclsmentioning

confidence: 99%

Targeting and processing of site‐specific DNA interstrand crosslinks

Vásquez

2010

Environ and Mol Mutagen

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DNA interstrand crosslinks (ICLs) are among the most cytotoxic types of DNA damage, and thus ICL-inducing agents such as cyclophosphamide, melphalan, cisplatin, psoralen and mitomycin C have been used clinically as anti-cancer drugs for decades. ICLs can also be formed endogenously as a consequence of cellular metabolic processes. ICL-inducing agents continue to be among the most effective chemotherapeutic treatments for many cancers; however, treatment with these agents can lead to secondary malignancies, in part due to mutagenic processing of the DNA lesions. The mechanisms of ICL repair have been characterized more thoroughly in bacteria and yeast than in mammalian cells. Thus, a better understanding the molecular mechanisms of ICL processing offers the potential to improve the efficacy of these drugs in cancer therapy. In mammalian cells it is thought that ICLs are repaired by the coordination of proteins from several pathways, including nucleotide excision repair (NER), base excision repair (BER), mismatch repair (MMR), homologous recombination (HR), translesion synthesis (TLS), and proteins involved in Fanconi anemia (FA). In this review, we focus on the potential functions of NER, MMR, and HR proteins in the repair of and response to ICLs in human cells and in mice. We will also discuss a unique approach, using psoralen covalently linked to triplex-forming oligonucleotides to direct ICLs to specific sites in the mammalian genome.

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Preferential binding of human XPA to the mitomycin C-DNA interstrand crosslink and modulation by arsenic and cadmium

Cited by 21 publications

References 27 publications

Impact of arsenic on nucleotide excision repair: XPC function, protein level, and gene expression

Impact of arsenic on nucleotide excision repair: XPC function, protein level, and gene expression

Initiation of DNA interstrand cross‐link repair in mammalian cells

Targeting and processing of site‐specific DNA interstrand crosslinks

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