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NER pathway

Luz I Valenzuela-García, Víctor M Ayala-García, Ana G Regalado-García, Peter Setlow, Mario Pedraza-Reyes
The absence of base excision repair (BER) proteins involved in processing ROS-promoted genetic insults activates a DNA damage scanning (DisA)-dependent checkpoint event in outgrowing Bacillus subtilis spores. Here, we report that genetic disabling of transcription-coupled repair (TCR) or nucleotide excision repair (NER) pathways severely affected outgrowth of ΔdisA spores, and much more so than the effects of these mutations on log phase growth. This defect delayed the first division of spore's nucleoid suggesting that unrepaired lesions affected transcription and/or replication during outgrowth...
March 13, 2018: MicrobiologyOpen
Barbara Bukowska, Boleslaw T Karwowski
The clustered DNA lesions are a characteristic feature of ionizing radiation and are defined as two or more damage sites formed within 20 bps after the passage of a single radiation track. The clustered DNA lesions are divided into two major groups: double-stranded breaks (DSBs) and non-DSB clusters also known as Oxidatively-induced Clustered DNA Lesions (OCDLs), which could involve either two opposing strands or the same strand. As irradiation is gaining greater interest in cancer treatment as well as in imaging techniques, the detailed knowledge of its genotoxicity and the mechanisms of repair of radiation-induced DNA damage remain issues to explore...
February 25, 2018: Current Medicinal Chemistry
Shalaka Chitale, Holger Richly
The integrity of the genome is maintained by specific DNA repair pathways. The main pathway removing DNA lesions induced by exposure to UV light is nucleotide excision repair (NER). The DNA damage response at chromatin is accompanied by the recruitment of DNA repair factors to the lesion site and the deposition of specific histone marks. The function of these histone marks in NER stays for the most part elusive. We have recently reported that the methyltransferase MMSET catalyzes the dimethylation of histone H4 at lysine 20 (H4K20me2) at the lesion site...
February 26, 2018: Nucleus
Marie-Catherine Drigeard Desgarnier, Patrick J Rochette
Absorption of solar ultraviolet (UV) radiation by DNA leads to the formation of the highly mutagenic cyclobutane pyrimidine dimer (CPD). The mutagenicity of CPD is caused, in part, by the fact that their recognition and repair by the nucleotide excision repair (NER) pathway is challenging and slow. It has been previously shown that a pre-stimulation with genotoxic agents improve NER efficiency of CPD, indicating a potential adaptive response of this repair pathway. We have pre-treated human dermal fibroblasts with repeated subletal low doses of UVB (chronic low-dose of UVB; CLUV) to determine whether it could enhance NER capacity to repair CPD...
March 2018: DNA Repair
Yunes Panahi, Amir Fattahi, Hamid Reza Nejabati, Sina Abroon, Zeinab Latifi, Abolfazl Akbarzadeh, Tohid Ghasemnejad
Sulfur mustard (SM) is an alkylating agent that causes severe damages to the skin, eyes, and the respiratory system. DNA alkylation is one of the most critical lesions that could lead to monoadducts and cross-links, as well as DNA strand breaks. In response to these adducts, cells initiate a series of reactions to recruit specific DNA repair pathways. The main DNA repair pathways in human cells, which could be involved in the DNA SM-induced DNA damages, are base excision repair (BER), nucleotide excision repair (NER), homologous recombination (HR) and non-homologous end joining (NHEJ)...
February 2, 2018: Environmental Toxicology and Pharmacology
Lisa N Chesner, Colin Campbell
DNA-protein crosslinks (DPCs) are complex DNA lesions that induce mutagenesis and cell death. DPCs are created by common antitumor drugs, reactive oxygen species, and endogenous aldehydes. Since these agents create other types of DNA damage in addition to DPCs, identification of the mechanisms of DPC repair is challenging. In this study, we created plasmid substrates containing site-specific DPC lesions, as well as plasmids harboring lesions that are selectively repaired by the base excision or nucleotide excision repair (NER) pathways...
January 9, 2018: DNA Repair
Janin Lehmann, Christina Seebode, Marie Christine Martens, Steffen Emmert
Ultraviolet (UV)-induced DNA lesions are almost exclusively removed by the nucleotide excision repair (NER) pathway, which is essential for prevention of skin cancer development. Patients with xeroderma pigmentosum (XP) are extremely sun sensitive due to a genetic defect in components of the NER cascade. They present with first signs of premature skin aging at an early age, with a considerably increased risk of developing UV-induced skin cancer. XP belongs to the group of DNA repair defective disorders that are mainly diagnosed in the clinic and in hindsight confirmed at the molecular level...
February 2018: Anticancer Research
Ou-Gen Liu, Xiao-Yan Xiong, Chun-Ming Li, Xian-Sheng Zhou, Si-Si Li
BACKGROUND Cutaneous squamous cell carcinoma (cSCC) is the second most widespread cancer in humans and its incidence is rising. Novel therapy with better efficacy is needed for clinical treatment of cSCC. Many studies have shown the importance of DNA repair pathways during the development of cancer. A key nucleotide excision repair (NER) protein, xeroderma pigmentosum group D (XPD), is responsible for the excision of a large variety of bulky DNA lesions. MATERIAL AND METHODS To explore the role of XPD in A431 cells, we overexpressed XPD in A431 cells and performed MTT assay, flow cytometry, and Western blot analysis to examine cell proliferation, cell apoptosis, and genes expression...
January 24, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
Yuliya S Krasikova, Nadejda I Rechkunova, Ekaterina A Maltseva, Olga I Lavrik
Replication protein A (RPA) and the xeroderma pigmentosum group A (XPA) protein are indispensable for both pathways of nucleotide excision repair (NER). Here we analyze the interaction of RPA and XPA with DNA containing a flap and different size gaps that imitate intermediates of the late NER stages. Using gel mobility shift assays, we found that RPA affinity for DNA decreased when DNA contained both extended gap and similar sized flap in comparison with gapped-DNA structure. Moreover, crosslinking experiments with the flap-gap DNA revealed that RPA interacts mainly with the ssDNA platform within the long gap and contacts flap in DNA with a short gap...
2018: PloS One
Barbara Bukowska, Bolesław T Karwowski
Xeroderma pigmentosum (XP), trichothiodystrophy (TTD) and Cockayne syndrome (CS) are rare genetic diseases characterized by a large range of clinical symptoms. However, they are all associated with defects in nucleotide excision repair (NER), the system responsible for removing bulky DNA lesions such as those generated by UV light: cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone photoproducts (6-4 PPs). Over the past years, detailed structural and biochemical information on NER-associated proteins has emerged...
January 2, 2018: Life Sciences
Yi Huo, Zhaoyun Zong, Qingtao Wang, Zhenyu Zhang, Haiteng Deng
Tumor cells frequently evolved resistance to cisplatin that greatly compromises the efficacy of chemotherapy. Identification of the mechanisms underlying drug resistance is important for developing new therapeutic approaches. ISG15 is found to be elevated in many human carcinomas and cancer cell lines. Here, we identified that the expressions of ISG15 and ISG15-conjugating system were downregulated in drug resistant A549/DDP cells compared to drug sensitive A549 cells. Silencing of ISG15 robustly elevated the resistance to cisplatin, suggesting ISG15 plays an important role in cisplatin resistance...
December 8, 2017: Oncotarget
Triparna Lahari, Janelle Lazaro, Dana F Schroeder
In plants, exposure to solar ultraviolet (UV) light is unavoidable, resulting in DNA damage. Damaged DNA causes mutations, replication arrest, and cell death, thus efficient repair of the damaged DNA is essential. A light-independent DNA repair pathway called nucleotide excision repair (NER) is conserved throughout evolution. For example, the damaged DNA-binding protein Radiation sensitive 4 (Rad4) in Saccharomyces cerevisiae is homologous to the mammalian NER protein Xeroderma Pigmentosum complementation group C (XPC)...
December 28, 2017: Genes
Jemma Hawkins, Michelle Edwards, Joanna Charles, Russell Jago, Mark Kelson, Kelly Morgan, Simon Murphy, Emily Oliver, Sharon Simpson, Rhiannon Tudor Edwards, Graham Moore
Background: Exercise referral schemes are recommended by the National Institute for Clinical Excellence (NICE) for physical activity promotion among inactive patients with health conditions or risk factors. Whilst there is evidence for the initial effectiveness and cost-effectiveness of such schemes for increasing physical activity, evidence of long-term effects is limited. Techniques such as goal setting, self-monitoring and personalised feedback may support motivation for physical activity...
2017: Pilot and Feasibility Studies
Shalaka Chitale, Holger Richly
Ultraviolet (UV) irradiation triggers the recruitment of DNA repair factors to the lesion sites and the deposition of histone marks as part of the DNA damage response. The major DNA repair pathway removing DNA lesions caused by exposure to UV light is nucleotide excision repair (NER). We have previously demonstrated that the endoribonuclease DICER facilitates chromatin decondensation during lesion recognition in the global-genomic branch of NER. Here, we report that DICER mediates the recruitment of the methyltransferase MMSET to the DNA damage site...
December 12, 2017: Journal of Cell Biology
Palak Shah, Lei Qiang, Seungwon Yang, Keyoumars Soltani, Yu-Ying He
Nucleotide excision repair (NER) is the most versatile DNA repair pathway for removing DNA damage caused by UV radiation and many environmental carcinogens. NER is essential for suppressing tumorigenesis in the skin, lungs and brain. Although the core NER proteins have been identified and characterized, molecular regulation of NER remains poorly understood. Here we show that ubiquitin-specific peptidase 11 (USP11) positively regulates NER by deubiquitinating xeroderma pigmentosum complementation group C (XPC) and promoting its retention at the DNA damage sites...
November 14, 2017: Oncotarget
Gerhard Hamilton, Barbara Rath
The efficacy of platinum-based chemotherapy for patients with non-small cell lung cancer (NSCLC) is limited by chemoresistance. Platinum drugs damage DNA by introducing intrastrand and interstrand crosslinks which result in cell death. Excision repair cross-complementing 1 (ERCC1) is a member of the nucleotide excision repair (NER) pathway which erases such defects. Single nucleotide polymorphisms (SNPs) in ERCC1 impair this activity and have been suggested to predict the response to chemotherapy. Area covered: Among the polymorphisms of proteins involved in uptake, metabolism, cytotoxicity and efflux of platinum drugs, codon 118 C/T and C8092A in ERCC1 are the best characterized SNPs studied for their predictive power...
January 2018: Expert Opinion on Drug Metabolism & Toxicology
Jianfeng Chen, Ningjie Sun, Gang Hu, Xiansheng Chen, Jiansong Jiang, Haiming Wu, Gaojian Luo
The ERCC1 enzyme in the nucleotide excision repair (NER) pathway plays a vital role in DNA repair. Numerous epidemiological studies have evaluated the association between ERCC1 polymorphisms and the risk of colorectal cancer (CRC), with conflicting results. To evaluate the potential associations, we conducted a meta-analysis. Eligible studies were identified by searching electronic databases. The odds ratio (OR) and 95% confidence interval (CI) were applied to assess the associations between ERCC1 polymorphisms and CRC risk...
2017: Critical Reviews in Eukaryotic Gene Expression
Amandeep Singh
The genomic integrity of Mycobacterium tuberculosis is continuously threatened by the harsh survival conditions inside host macrophages, due to immune and antibiotic stresses. Faithful genome maintenance and repair must be accomplished under stress for the bacillus to survive in the host, necessitating a robust DNA repair system. The importance of DNA repair systems in pathogenesis is well established. Previous examination of the M. tuberculosis genome revealed homologues of almost all the major DNA repair systems, i...
December 2017: Microbiology
Abdelghani Mazouzi, Federica Battistini, Sarah C Moser, Joana Ferreira da Silva, Marc Wiedner, Michel Owusu, Charles-Hugues Lardeau, Anna Ringler, Beatrix Weil, Jürgen Neesen, Modesto Orozco, Stefan Kubicek, Joanna I Loizou
DNA lesions caused by UV damage are thought to be repaired solely by the nucleotide excision repair (NER) pathway in human cells. Patients carrying mutations within genes functioning in this pathway display a range of pathologies, including an increased susceptibility to cancer, premature aging, and neurological defects. There are currently no curative therapies available. Here we performed a high-throughput chemical screen for agents that could alleviate the cellular sensitivity of NER-deficient cells to UV-induced DNA damage...
November 16, 2017: Molecular Cell
Ruoxin Zhang, Ming Jia, Yuan Xu, Danwen Qian, Mengyun Wang, Meiling Zhu, Menghong Sun, Jianhua Chang, Qingyi Wei
Platinum-based chemotherapy (PBC) in combination with the 3(rd) generation drugs is the first-line treatment for patients with advanced non-small cell lung cancer (NSCLC); however, the efficacy is severely hampered by grade 3-4 toxicities. Nucleotide excision repair (NER) pathway is the main mechanism of removing platinum-induced DNA adducts, contributing to the toxicity and outcome of PBC. We analyzed data from 710 Chinese NSCLC patients treated with PBC and assessed the associations of 25 potentially functional single nucleotide polymorphisms (SNPs) in eight NER core genes with overall, gastrointestinal and hematologic toxicities...
November 14, 2017: International Journal of Cancer. Journal International du Cancer
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