scholarly journals Identification of Novel Interaction Partners of Ets-1: Focus on DNA Repair

Genes ◽  
2019 ◽  
Vol 10 (3) ◽  
pp. 206
Author(s):  
Guillaume Brysbaert ◽  
Jérôme de Ruyck ◽  
Marc Aumercier ◽  
Marc F. Lensink
Keyword(s):  
Dna Repair ◽  
Interaction Model ◽  
Protein Docking ◽  
Dna Repair Enzymes ◽  
Dna Repair Mechanisms ◽  
Repair Enzymes ◽  
Repair Mechanisms ◽  
Important Regulator ◽  
Dependent Protein ◽  
Parp 1

The transcription factor Ets-1 (ETS proto-oncogene 1) shows low expression levels except in specific biological processes like haematopoiesis or angiogenesis. Elevated levels of expression are observed in tumor progression, resulting in Ets-1 being named an oncoprotein. It has recently been shown that Ets-1 interacts with two DNA repair enzymes, PARP-1 (poly(ADP-ribose) polymerase 1) and DNA-PK (DNA-dependent protein kinase), through two different domains and that these interactions play a role in cancer. Considering that Ets-1 can bind to distinctly different domains of two DNA repair enzymes, we hypothesized that the interaction can be transposed onto homologs of the respective domains. We have searched for sequence and structure homologs of the interacting ETS(Ets-1), BRCT(PARP-1) and SAP(DNA-PK) domains, and have identified several candidate binding pairs that are currently not annotated as such. Many of the Ets-1 partners are associated to DNA repair mechanisms. We have applied protein-protein docking to establish putative interaction poses and investigated these using centrality analyses at the protein residue level. Most of the identified poses are virtually similar to our recently established interaction model for Ets-1/PARP-1 and Ets-1/DNA-PK. Our work illustrates the potentially high number of interactors of Ets-1, in particular involved in DNA repair mechanisms, which shows the oncoprotein as a potential important regulator of the mechanism.

scholarly journals Coordinated signals from the DNA repair enzymes PARP-1 and PARP-2 promotes B-cell development and function

2019 ◽  
Vol 26 (12) ◽  
pp. 2667-2681 ◽  
Author(s):  
Miguel A. Galindo-Campos ◽  
Marie Bedora-Faure ◽  
Jordi Farrés ◽  
Chloé Lescale ◽  
Lucia Moreno-Lama ◽  
...  
Keyword(s):  
Dna Repair ◽  
B Cell ◽  
Cell Development ◽  
B Cell Development ◽  
Dna Repair Enzymes ◽  
Repair Enzymes ◽  
And Function ◽  
Parp 1

scholarly journals Sensitizing Ewing sarcoma to chemo- and radiotherapy by inhibition of the DNA-repair enzymes DNA protein kinase (DNA-PK) and poly-ADP-ribose polymerase (PARP) 1/2

Oncotarget ◽  
2017 ◽  
Vol 8 (69) ◽  
pp. 113418-113430 ◽  
Author(s):  
Britta Vormoor ◽  
Yvonne T. Schlosser ◽  
Helen Blair ◽  
Abhishek Sharma ◽  
Sarah Wilkinson ◽  
...  
Keyword(s):  
Dna Repair ◽  
Protein Kinase ◽  
Ewing Sarcoma ◽  
Dna Repair Enzymes ◽  
Repair Enzymes ◽  
Parp 1

scholarly journals Renewing DNA integrity by cell repair systems

2018 ◽  
Vol 23 ◽  
pp. 208-213
Author(s):  
L. L. Lukash
Keyword(s):  
Dna Repair ◽  
Eukaryotic Cells ◽  
Dna Integrity ◽  
Endogenous Factors ◽  
Cell Repair ◽  
Dna Repair Mechanisms ◽  
Repair Enzymes ◽  
Repair Mechanisms ◽  
The Common ◽  
Repair Systems

The four of six main cell repair systems have been reviewed. Some of them have been studied by Nobel laureates of 2015 year in the field of chemistry. The common title of their work is “For investigation of DNA repair mechanisms”. Numerous primer damages of DNA induced by exogenous and endogenous factors are corrected by complex cell systems including repair enzymes and other proteins. Mutational changes in the genes coding the repair enzymes are the most dangerous because they dramatically increase mutation frequency in pro- and eukaryotic cells. But due to the constant and correct action of cell repair enzymes DNA integrity is renewing, that is why the organisms on our planet are still alive and functionally active. Keywords: DNA repair, reparative enzymes, pro- and eukaryotic cells, primer damages, mutations.

Asbestos-Induced Pulmonary Toxicity: Role of DNA Damage and Apoptosis

2003 ◽  
Vol 228 (6) ◽  
pp. 650-659 ◽  
Author(s):  
Daya Upadhyay ◽  
David W. Kamp
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Death Receptor ◽  
Target Cells ◽  
Strand Breaks ◽  
Dna Repair Mechanisms ◽  
Repair Enzymes ◽  
Repair Mechanisms ◽  
The Face ◽  
Dna Strand

Asbestos causes asbestosis and various malignancies by mechanisms that are not clearly defined. Here, we review the accumulating evidence showing that asbestos is directly genotoxic by inducing DNA strand breaks (DNA-SB) and apoptosis in relevant lung target cells. Although the exact mechanisms by which asbestos causes DNA damage and apoptosis are not firmly established, some of the implicated mechanisms include the generation of iron-derived reactive oxygen species (ROS) as well as reactive nitrogen species (RNS), alteration in the mitochondrial function, and activation of the death receptor pathway. We focus on the accumulating evidence implicating ROS. DNA repair mechanisms have a key role in limiting the extent of DNA damage. Recent studies show that asbestos activates DNA repair enzymes such as apurinic/apyrimidinic endonuclease (APE) and poly (ADP-ribose) polymerase (PARP). Asbestos-induced neoplastic transformation may result in the setting where DNA damage overwhelms DNA repair in the face of a persistent proliferative signal. Strategies aimed at limiting asbestos-induced oxidative stress may reduce DNA damage and, as such, prevent malignant transformation.

scholarly journals DASH-type cryptochromes – solved and open questions

2020 ◽  
Vol 401 (12) ◽  
pp. 1487-1493
Author(s):  
Stephan Kiontke ◽  
Tanja Göbel ◽  
Annika Brych ◽  
Alfred Batschauer
Keyword(s):  
Dna Repair ◽  
Circadian Clock ◽  
Blue Light ◽  
Dna Repair Enzymes ◽  
Repair Enzymes ◽  
Open Questions ◽  
Essential Components ◽  
Repair Activity ◽  
Almost All ◽  
Uv Lesions

AbstractDrosophila, Arabidopsis, Synechocystis, human (DASH)-type cryptochromes (cry-DASHs) form one subclade of the cryptochrome/photolyase family (CPF). CPF members are flavoproteins that act as DNA-repair enzymes (DNA-photolyases), or as ultraviolet(UV)-A/blue light photoreceptors (cryptochromes). In mammals, cryptochromes are essential components of the circadian clock feed-back loop. Cry-DASHs are present in almost all major taxa and were initially considered as photoreceptors. Later studies demonstrated DNA-repair activity that was, however, restricted to UV-lesions in single-stranded DNA. Very recent studies, particularly on microbial organisms, substantiated photoreceptor functions of cry-DASHs suggesting that they could be transitions between photolyases and cryptochromes.

scholarly journals DNA Damage Response in Multiple Myeloma: The Role of the Tumor Microenvironment

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 504
Author(s):  
Takayuki Saitoh ◽  
Tsukasa Oda
Keyword(s):  
Multiple Myeloma ◽  
Dna Damage ◽  
Dna Repair ◽  
Tumor Microenvironment ◽  
Dna Damage Response ◽  
Genetic Instability ◽  
Dna Repair Mechanisms ◽  
Damage Response ◽  
Repair Mechanisms

Multiple myeloma (MM) is an incurable plasma cell malignancy characterized by genomic instability. MM cells present various forms of genetic instability, including chromosomal instability, microsatellite instability, and base-pair alterations, as well as changes in chromosome number. The tumor microenvironment and an abnormal DNA repair function affect genetic instability in this disease. In addition, states of the tumor microenvironment itself, such as inflammation and hypoxia, influence the DNA damage response, which includes DNA repair mechanisms, cell cycle checkpoints, and apoptotic pathways. Unrepaired DNA damage in tumor cells has been shown to exacerbate genomic instability and aberrant features that enable MM progression and drug resistance. This review provides an overview of the DNA repair pathways, with a special focus on their function in MM, and discusses the role of the tumor microenvironment in governing DNA repair mechanisms.

scholarly journals Ancient Sturgeons Possess Effective DNA Repair Mechanisms: Influence of Model Genotoxicants on Embryo Development of Sterlet, Acipenser ruthenus

2020 ◽  
Vol 22 (1) ◽  
pp. 6
Author(s):  
Ievgeniia Gazo ◽  
Roman Franěk ◽  
Radek Šindelka ◽  
Ievgen Lebeda ◽  
Sahana Shivaramu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Damage ◽  
Dna Repair ◽  
Embryo Development ◽  
Hatching Rate ◽  
Embryo Survival ◽  
Dna Repair Mechanisms ◽  
Acipenser Ruthenus ◽  
Repair Mechanisms ◽  
Sterlet Acipenser Ruthenus

DNA damage caused by exogenous or endogenous factors is a common challenge for developing fish embryos. DNA damage repair (DDR) pathways help organisms minimize adverse effects of DNA alterations. In terms of DNA repair mechanisms, sturgeons represent a particularly interesting model due to their exceptional genome plasticity. Sterlet (Acipenser ruthenus) is a relatively small species of sturgeon. The goal of this study was to assess the sensitivity of sterlet embryos to model genotoxicants (camptothecin, etoposide, and benzo[a]pyrene), and to assess DDR responses. We assessed the effects of genotoxicants on embryo survival, hatching rate, DNA fragmentation, gene expression, and phosphorylation of H2AX and ATM kinase. Exposure of sterlet embryos to 1 µM benzo[a]pyrene induced low levels of DNA damage accompanied by ATM phosphorylation and xpc gene expression. Conversely, 20 µM etoposide exposure induced DNA damage without activation of known DDR pathways. Effects of 10 nM camptothecin on embryo development were stage-specific, with early stages, before gastrulation, being most sensitive. Overall, this study provides foundational information for future investigation of sterlet DDR pathways.

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