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https://www.readbyqxmd.com/read/28818580/effects-of-sulfur-mustard-on-mesenchymal-stem-cells
#1
Annette Schmidt, Steinritz Dirk, Rothmiller Simone, Thiermann Horst, Scherer A Michael
Chronic wound healing disorders that occur as a result of a sulfur mustard (SM) exposure present a particular challenge. These chronic wounds are similar to other chronic wounds. In the past, it has been shown that mesenchymal stem cells (MSC) play an important role in the healing of chronic wounds. An important property to support wound healing is their ability to migrate. However, we were able to show that SM leads to a reduction in MSC migration even at low concentrations. Currently, exposed MSCs are still able to differentiate...
August 14, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/28813038/prostate-cancer-a-variety-of-therapy-arvs-mediate-ddr
#2
Louise Stone
No abstract text is available yet for this article.
August 16, 2017: Nature Reviews. Urology
https://www.readbyqxmd.com/read/28811338/emerging-functions-of-the-fanconi-anemia-pathway-at-a-glance
#3
REVIEW
Rhea Sumpter, Beth Levine
Fanconi anemia (FA) is a rare disease, in which homozygous or compound heterozygous inactivating mutations in any of 21 genes lead to genomic instability, early-onset bone marrow failure and increased cancer risk. The FA pathway is essential for DNA damage response (DDR) to DNA interstrand crosslinks. However, proteins of the FA pathway have additional cytoprotective functions that may be independent of DDR. We have shown that many FA proteins participate in the selective autophagy pathway that is required for the destruction of unwanted intracellular constituents...
August 15, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28808232/analysis-of-the-atr-chk1-and-atm-chk2-pathways-in-male-breast-cancer-revealed-the-prognostic-significance-of-atr-expression
#4
Anna Di Benedetto, Cristiana Ercolani, Marcella Mottolese, Francesca Sperati, Laura Pizzuti, Patrizia Vici, Irene Terrenato, Abeer M Shaaban, Matthew P Humphries, Luigi Di Lauro, Maddalena Barba, Ilio Vitale, Gennaro Ciliberto, Valerie Speirs, Ruggero De Maria, Marcello Maugeri-Saccà
The ATR-Chk1 and ATM-Chk2 pathways are central in DNA damage repair (DDR) and their over-activation may confer aggressive molecular features, being an adaptive response to endogenous DNA damage and oncogene-induced replication stress. Herein we investigated the ATR-Chk1 and ATM-Chk2 signalings in male breast cancer (MBC). The expression of DDR kinases (pATR, pATM, pChk1, pChk2, and pWee1) and DNA damage markers (pRPA32 and γ-H2AX) was evaluated by immunohistochemistry in 289 MBC samples to assess their association...
August 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28796247/p53-dependent-downregulation-of-htert-protein-expression-and-telomerase-activity-induces-senescence-in-lung-cancer-cells-as-a-result-of-pterostilbene-treatment
#5
Rong-Jane Chen, Pei-Hsuan Wu, Chi-Tang Ho, Tzong-Der Way, Min-Hsiung Pan, Hsiu-Min Chen, Yuan-Soon Ho, Ying-Jan Wang
Cellular senescence is characterized by permanent cell cycle arrest, triggered by a variety of stresses, such as telomerase inhibition, and it is recognized as a tumor-suppressor mechanism. In recent years, telomerase has become an important therapeutic target in several cancers; inhibition of telomerase can induce senescence via the DNA damage response (DDR). Pterostilbene (PT), a dimethyl ether analog of resveratrol, possesses a variety of biological functions, including anticancer effects; however, the molecular mechanisms underlying these effects are not fully understood...
August 10, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28794020/adenovirus-core-protein-vii-down-regulates-the-dna-damage-response-on-the-host-genome
#6
Daphne C Avgousti, Ashley N Della Fera, Clayton J Otter, Christin Herrmann, Neha J Pancholi, Matthew D Weitzman
Viral manipulation of cellular proteins allows viruses to suppress host defenses and generate infectious progeny. Due to the linear double-stranded DNA nature of the adenovirus genome, the cellular DNA damage response (DDR) is considered a barrier for successful infection. The adenovirus genome is packaged with protein VII, a viral-encoded histone-like core protein that is suggested to protect incoming viral genomes from detection by cellular DNA damage machinery. We showed that protein VII localizes to host chromatin during infection, leading us to hypothesize that protein VII may affect DNA damage responses on the cellular genome...
August 9, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28791382/potential-role-of-zeb1-as-a-dna-repair-regulator-in-colorectal-cancer-cells-revealed-by-cancer-associated-promoter-profiling
#7
Miao Wang, Su-Fei He, Lei-Lei Liu, Xiao-Xia Sun, Fan Yang, Qian Ge, Wei-Kang Wong, Jing-Yan Meng
Besides being a key contributor to epithelial‑to‑mesenchymal transition (EMT) activation and stemness maintenance, zinc finger E-box binding homeobox 1 (ZEB1) is also a crucial inducer of chemoresistance and radioresistance. Unlike the clear mechanism that mediates its effect on EMT and dedifferentiation, the mechanism of how ZEB1 promotes chemo- and radio-resistance remains to be elucidated. It has been previously reported that ZEB1 promotes DNA double-strand break clearance by enhancing the deubiquitylating activity of ubiquitin-specific peptidase (USP)7 on checkpoint kinase 1, which is an important step during DNA repair...
August 8, 2017: Oncology Reports
https://www.readbyqxmd.com/read/28783563/stimulation-of-rna-polymerase-ii-ubiquitination-and-degradation-by-yeast-mrna-3-end-processing-factors-is-a-conserved-dna-damage-response-in-eukaryotes
#8
Jason N Kuehner, James W Kaufman, Claire Moore
The quality and retrieval of genetic information is imperative to the survival and reproduction of all living cells. Ultraviolet (UV) light induces lesions that obstruct DNA access during transcription, replication, and repair. Failure to remove UV-induced lesions can abrogate gene expression and cell division, resulting in permanent DNA mutations. To defend against UV damage, cells utilize transcription-coupled nucleotide excision repair (TC-NER) to quickly target lesions within active genes. In cases of long-term genotoxic stress, a slower alternative pathway promotes degradation of RNA Polymerase II (Pol II) to allow for global genomic nucleotide excision repair (GG-NER)...
July 23, 2017: DNA Repair
https://www.readbyqxmd.com/read/28783053/regulation-of-dna-repair-mechanisms-how-the-chromatin-environment-regulates-the-dna-damage-response
#9
REVIEW
Jens Stadler, Holger Richly
Cellular DNA is constantly challenged by damage-inducing factors derived from exogenous or endogenous sources. In order to maintain genome stability and integrity, cells have evolved a wide variety of DNA repair pathways which counteract different types of DNA lesions, also referred to as the DNA damage response (DDR). However, DNA in eukaryotes is highly organized and compacted into chromatin representing major constraints for all cellular pathways, including DNA repair pathways, which require DNA as their substrate...
August 5, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28779964/the-c-elegans-set-2-set1-histone-h3-lys4-h3k4-methyltransferase-preserves-genome-stability-in-the-germline
#10
M Herbette, M G Mercier, F Michal, D Cluet, C Burny, G Yvert, V J Robert, F Palladino
Maintaining the integrity of genetic information across generations is essential for both cell survival and reproduction, and requires the timely repair of DNA damage. Histone-modifying enzymes play a central role in the DNA repair process through the deposition and removal of post-translational modifications on the histone tails. Specific histone modification act in the DNA repair process through the recruitment of proteins and complexes with specific enzymatic activities, or by altering the chromatin state at the site of DNA lesions...
July 29, 2017: DNA Repair
https://www.readbyqxmd.com/read/28764946/balancing-act-to-be-or-not-to-be-ubiquitylated
#11
REVIEW
Ryotaro Nishi
DNA double-strand breaks (DSBs) are one of the most deleterious DNA lesions. Appropriate repair of DSB either by homologous recombination or non-homologous end-joining is critical for maintaining genome stability and fitness. DSB repair cooperates with cellular signalling networks, namely DSB response (DDR), which plays pivotal roles in the choice of DSB repair pathway, orchestrating recruitment of DDR factors to site of damage, transcription suppression and cell cycle checkpoint activation. It has been revealed that these mechanisms are strictly regulated, in time and space, by complex and minute ubiquitylation-mediated reactions...
July 21, 2017: Mutation Research
https://www.readbyqxmd.com/read/28759035/sall4-promotes-glycolysis-and-chromatin-remodeling-via-modulating-hp1%C3%AE-glut1-pathway
#12
J Kim, S Xu, L Xiong, L Yu, X Fu, Y Xu
SALL4 has recently been identified to promote chemo-resistance in multiple types of cancer, but the underlying mechanism remains to be fully established. Open chromatin structure is important for DNA damage response (DDR) and DNA repair. Here, we demonstrate that SALL4 promotes open chromatin by destabilizing heterochromatin protein 1α (HP1α) by recruiting ubiquitin E3 ligase CUL4B to HP1α. The silencing of SALL4 in cancer cells decreased the expression levels of Glut1 and inhibited glycolysis in cancer cells...
July 31, 2017: Oncogene
https://www.readbyqxmd.com/read/28758831/tet1-deficiency-attenuates-the-dna-damage-response-and-promotes-resistance-to-dna-damaging-agents
#13
Jonathan B Coulter, Hernando Lopez-Bertoni, Katherine J Kuhns, Richard S Lee, John Laterra, Joseph P Bressler
Recent studies have shown that loss of TET1 may play a significant role in the formation of tumors. Because genomic instability is a hallmark of cancer, we examined the potential involvement of ten-eleven translocation 1 (TET1) in the DNA damage response (DDR). Here we demonstrate that, in response to clinically relevant doses of ionizing radiation (IR), human glial cells made TET1-deficient with lentiviral vectors displayed greater numbers of colony forming units and lower levels of apoptotic markers compared to glial cells transduced with control vectors; yet, they harbored greater DNA strand breaks...
July 31, 2017: Epigenetics: Official Journal of the DNA Methylation Society
https://www.readbyqxmd.com/read/28754843/hormone-induced-dna-damage-response-and-repair-mediated-by-cyclin-d1-in-breast-and-prostate-cancer
#14
REVIEW
Gabriele Di Sante, Agnese Di Rocco, Claudia Pupo, Mathew C Casimiro, Richard G Pestell
Cell cycle control proteins govern events that leads to the production of two identical daughter cells. Distinct sequential temporal phases, Gap 1 (G1), Gap 0 (G0), Synthesis (S), Gap 2 (G2) and Mitosis (M) are negotiated through a series of check points during which the favorability of the local cellular environment is assessed, prior to replicating DNA [1]. Cyclin D1 has been characterized as a key regulatory subunit of the holoenzyme that promotes the G1/S-phase transition through phosphorylating the pRB protein...
July 20, 2017: Oncotarget
https://www.readbyqxmd.com/read/28754673/androgen-receptor-variants-mediate-dna-repair-after-prostate-cancer-irradiation
#15
Yi Yin, Rui Li, Kangling Xu, Sentai Ding, Jeffrey Li, Guemhee Baek, Susmita G Ramanand, Sam Ding, Zhao Liu, Yunpeng Gao, Mohammed S Kanchwala, Xiangyi Li, Ryan Hutchinson, Xihui Liu, Solomon L Woldu, Chao Xing, Neil B Desai, Felix Y Feng, Sandeep Burma, Johann S de Bono, Scott M Dehm, Ram S Mani, Benjamin P C Chen, Ganesh V Raj
In prostate cancer (PCa), androgen deprivation therapy (ADT) enhances the cytotoxic effects of radiotherapy. This effect is associated with weakening of the DNA damage response (DDR) normally supported by the androgen receptor. Since a significant number of patients will fail combined ADT and radiotherapy, we hypothesized that DDR may be driven by androgen receptor splice variants (ARV) induced by ADT. Investigating this hypothesis, we found that ARV increase the clonogenic survival of PCa cells after irradiation in an ADT-independent manner...
July 28, 2017: Cancer Research
https://www.readbyqxmd.com/read/28751499/dna-damage-signalling-in-d-melanogaster-requires-non-apoptotic-function-of-initiator-caspase-dronc
#16
Chaitali Khan, Sonia Muliyil, Champakali Ayyub, B J Rao
ϒH2Av response constitutes an important signalling event in DNA damage sensing ensuring effective repair by recruiting DNA repair machinery. In contrast, the occurrence of ϒH2Av response has also been reported in dying cells where it is shown to require activation of CAD (caspase activated DNase). Moreover, caspases are known to be required downstream of DNA damage for cell death execution. We show, for the first time, that initiator caspase Dronc, independent of executioner caspases, acts as an upstream regulator of DNA Damage Response (DDR) by facilitating ϒH2Av signalling perhaps involving non-apoptotic function...
July 27, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28734548/ubiquitin-like-modifications-in-the-dna-damage-response
#17
REVIEW
Zhifeng Wang, Wei-Guo Zhu, Xingzhi Xu
Genomic DNA is damaged at an extremely high frequency by both endogenous and environmental factors. An improper response to DNA damage can lead to genome instability, accelerate the aging process and ultimately cause various human diseases, including cancers and neurodegenerative disorders. The mechanisms that underlie the cellular DNA damage response (DDR) are complex and are regulated at many levels, including at the level of post-translational modification (PTM). Since the discovery of ubiquitin in 1975 and ubiquitylation as a form of PTM in the early 1980s, a number of ubiquitin-like modifiers (UBLs) have been identified, including small ubiquitin-like modifiers (SUMOs), neural precursor cell expressed, developmentally down-regulated 8 (NEDD8), interferon-stimulated gene 15 (ISG15), human leukocyte antigen (HLA)-F adjacent transcript 10 (FAT10), ubiquitin-fold modifier 1 (UFRM1), URM1 ubiquitin-related modifier-1 (URM1), autophagy-related protein 12 (ATG12), autophagy-related protein 8 (ATG8), fan ubiquitin-like protein 1 (FUB1) and histone mono-ubiquitylation 1 (HUB1)...
July 11, 2017: Mutation Research
https://www.readbyqxmd.com/read/28718433/mitotic-dna-damage-response-at-the-crossroads-of-structural-and-numerical-cancer-chromosome-instabilities
#18
REVIEW
Samuel F Bakhoum, Lilian Kabeche, Duane A Compton, Simon N Powell, Holger Bastians
DNA double-strand breaks (DSBs) prevent cells from entering mitosis allowing cells to repair their genomic damage. Little is known about the response to DSBs once cells have already committed to mitosis. Here, we review the genome-protective role of the mitotic DNA damage response (DDR) and evidence suggesting that its untimely activation induces chromosome segregation errors and paradoxically undermines genomic integrity. In contrast to normal cells, cancer cells coopt this pathway to propagate structural and numerical chromosomal instabilities...
March 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28713336/development-and-use-of-a-real-time-quantitative-pcr-method-for-detecting-and-quantifying-equol-producing-bacteria-in-human-faecal-samples-and-slurry-cultures
#19
Lucía Vázquez, Lucía Guadamuro, Froilán Giganto, Baltasar Mayo, Ana B Flórez
This work introduces a novel real-time quantitative PCR (qPCR) protocol for detecting and quantifying equol-producing bacteria. To this end, two sets of primers targeting the dihydrodaidzein reductase (ddr) and tetrahydrodaidzein reductase (tdr) genes, which are involved in the synthesis of equol, were designed. The primers showed high specificity and sensitivity when used to examine DNA from control bacteria, such as Slackia isoflavoniconvertens, Slackia equolifaciens, Asaccharobacter celatus, Adlercreutzia equolifaciens, and Enterorhabdus mucosicola...
2017: Frontiers in Microbiology
https://www.readbyqxmd.com/read/28707218/the-dna-damage-response-pathway-in-normal-hematopoiesis-and-malignancies
#20
REVIEW
Domenico Delia, Shuki Mizutani
In mammalian cells, the DNA damage response (DDR) prevents the replication and propagation of DNA errors to the next generation, thus maintaining genomic stability. At the heart of the DDR are the related signaling kinases ATM, ATR, and DNA-PK, which regulate DNA repair and associated events such as cell cycle checkpoints, chromatin remodeling, transcription, and ultimately apoptosis. Several findings highlight the occurrence of DDR in hemopoietic stem cells (HSCs), and persistence of DNA lesions in these cells promotes their functional decline and accumulation of leukemogenic mutations...
July 13, 2017: International Journal of Hematology
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