The ADP-ribosyltransferase PARP10/ARTD10 Interacts with Proliferating Cell Nuclear Antigen (PCNA) and Is Required for DNA Damage Tolerance

Nicolae, Claudia M.; Aho, Erin R.; Vlahos, Alexander H.S.; Choe, Katherine N.; De, Subhajyoti; Karras, Georgios I.; Moldovan, George‐Lucian

doi:10.1074/jbc.m114.556340

Cited by 91 publications

(121 citation statements)

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“…This is relevant because recent studies have linked MARylating ARTDs (mARTDs) to cancer biology . Notably, ARTD10/PARP10 has been suggested to be a potential drug target in cancer (Nicolae et al, 2014). Together these findings delineate the need to understand the cellular roles of the different PARylating and MARylating ARTDs and to develop tools to selectively modulate individual family members for functional studies and therapeutic approaches.…”

Section: Introductionmentioning

confidence: 94%

“…This results in inhibition of S phase and causes stalled replication forks (Koç et al, 2004). ARTD10 knockdown cells are more sensitive to HU-induced DNA damage as the catalytic activity is necessary for its DNA repair functions (Nicolae et al, 2014). We investigated whether we could reproduce this effect in HeLa cells using OUL35.…”

Section: Hydroxyurea Sensitivity Confirms the Role Of Artd10 In Genotmentioning

confidence: 99%

“…While some ARTDs modify substrates by transferring iteratively multiple ADP-ribose units resulting in poly-ADP-ribosylation (PARylation), most ARTDs mono-ADP-ribosylate (MARylate) their substrates (Kleine et al, 2008). ARTDs function in DNA damage repair (Malanga and Althaus, 2005;Nicolae et al, 2014Nicolae et al, , 2015, the unfolded protein response (Jwa and Chang, 2012), apoptosis Koh et al, 2005), heat shock (Petesch and Lis, 2008), cellular signaling (Feijs et al, 2013a;, cell division (Chang et al, 2004(Chang et al, , 2005(Chang et al, , 2009Ha et al, 2012), as well as transcription and chromatin regulation Schreiber et al, 2006). PARylating ARTDs (pARTDs; ARTD1-6), most prominently ARTD1, have been the focus of cancer related research during the past two decades.…”

Section: Introductionmentioning

confidence: 99%

“…A recent study has shown that ARTD10 interacts with PCNA and actively participates in S phase DNA damage repair by responding to replication fork stalling and activating translesion DNA synthesis (Nicolae et al, 2014). The exact mechanism of how ARTD10 is involved in this process is not clearly understood, but catalytic activity is needed for its DNA damage related functions (Nicolae et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…The exact mechanism of how ARTD10 is involved in this process is not clearly understood, but catalytic activity is needed for its DNA damage related functions (Nicolae et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Small-Molecule Chemical Probe Rescues Cells from Mono-ADP-Ribosyltransferase ARTD10/PARP10-Induced Apoptosis and Sensitizes Cancer Cells to DNA Damage

Venkannagari

Verheugd

Koivunen

et al. 2016

Cell Chemical Biology

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SUMMARYMembers of the human diphtheria toxin-likeADP-ribosyltransferase (ARTD or PARP) family play important roles in regulating biological activities by mediating either a mono-ADP-ribosylation MARylation) of a substrate or a poly-ADP-ribosylation (PARylation). ARTD10/PARP10 belongs to the MARylating ARTDs (mARTDs) subfamily, and plays important roles in biological processes that range from cellular signaling, DNA repair, and cell proliferation to immune response. Despite their biological and disease relevance, no selective inhibitors for mARTDs are available. Here we describe a small-molecule ARTD10 inhibitor, OUL35, a selective and potent inhibitor for this enzyme. We characterize its selectivity profile, model its binding, and demonstrate activity in HeLa cells where OUL35 rescued cells from ARTD10 induced cell death. Using OUL35 as a cell biology tool we show that ARTD10 inhibition sensitizes the cells to the hydroxyurea-induced genotoxic stress. Our study supports the proposed role of ARTD10 in DNA-damage repair and provides a tool compound for selective inhibition of ARTD10-mediated MARylation.3

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Section: Introductionmentioning

confidence: 94%

Section: Hydroxyurea Sensitivity Confirms the Role Of Artd10 In Genotmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…The exact mechanism of how ARTD10 is involved in this process is not clearly understood, but catalytic activity is needed for its DNA damage related functions (Nicolae et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Small-Molecule Chemical Probe Rescues Cells from Mono-ADP-Ribosyltransferase ARTD10/PARP10-Induced Apoptosis and Sensitizes Cancer Cells to DNA Damage

Venkannagari

Verheugd

Koivunen

et al. 2016

Cell Chemical Biology

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Identification of a genetic signature enriching for response to ibrutinib in relapsed/refractory follicular lymphoma in the DAWN phase 2 trial

et al. 2021

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Regulation of translesion DNA synthesis in mammalian cells

Tang

Guo

2020

Environ and Mol Mutagen

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The genomes of all living cells are under endogenous and exogenous attacks every day, causing diverse genomic lesions. Most of the lesions can be timely repaired by multiple DNA repair pathways. However, some may persist during S‐phase, block DNA replication, and challenge genome integrity. Eukaryotic cells have evolved DNA damage tolerance (DDT) to mitigate the lethal effects of arrested DNA replication without prior removal of the offending DNA damage. As one important mode of DDT, translesion DNA synthesis (TLS) utilizes multiple low‐fidelity DNA polymerases to incorporate nucleotides opposite DNA lesions to maintain genome integrity. Three different mechanisms have been proposed to regulate the polymerase switching between high‐fidelity DNA polymerases in the replicative machinery and one or more specialized enzymes. Additionally, it is known that proliferating cell nuclear antigen (PCNA) mono‐ubiquitination is essential for optimal TLS. Given its error‐prone property, TLS is closely associated with spontaneous and drug‐induced mutations in cells, which can potentially lead to tumorigenesis and chemotherapy resistance. Therefore, TLS process must be tightly modulated to avoid unwanted mutagenesis. In this review, we will focus on polymerase switching and PCNA mono‐ubiquitination, the two key events in TLS pathway in mammalian cells, and summarize current understandings of regulation of TLS process at the levels of protein–protein interactions, post‐translational modifications as well as transcription and noncoding RNAs. Environ. Mol. Mutagen. 61:680–692, 2020. © 2020 Wiley Periodicals, Inc.

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The ADP-ribosyltransferase PARP10/ARTD10 Interacts with Proliferating Cell Nuclear Antigen (PCNA) and Is Required for DNA Damage Tolerance

Cited by 91 publications

References 58 publications

Small-Molecule Chemical Probe Rescues Cells from Mono-ADP-Ribosyltransferase ARTD10/PARP10-Induced Apoptosis and Sensitizes Cancer Cells to DNA Damage

Small-Molecule Chemical Probe Rescues Cells from Mono-ADP-Ribosyltransferase ARTD10/PARP10-Induced Apoptosis and Sensitizes Cancer Cells to DNA Damage

Identification of a genetic signature enriching for response to ibrutinib in relapsed/refractory follicular lymphoma in the DAWN phase 2 trial

Regulation of translesion DNA synthesis in mammalian cells

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