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https://www.readbyqxmd.com/read/28088539/the-dna-damage-response-of-c-elegans-affected-by-gravity-sensing-and-radiosensitivity-during-the-shenzhou-8-spaceflight
#1
Ying Gao, Dan Xu, Lei Zhao, Yeqing Sun
Space radiation and microgravity are recognized as primary and inevitable risk factors for humans traveling in space, but the reports regarding their synergistic effects remain inconclusive and vary across studies due to differences in the environmental conditions and intrinsic biological sensitivity. Thus, we studied the synergistic effects on transcriptional changes in the global genome and DNA damage response (DDR) by using dys-1 mutant and ced-1 mutant of C. elegans, which respectively presented microgravity-insensitivity and radiosensitivity when exposure to spaceflight condition (SF) and space radiation (SR)...
January 7, 2017: Mutation Research
https://www.readbyqxmd.com/read/28075014/knockdown-of-rev3-synergizes-with-atr-inhibition-to-promote-apoptosis-induced-by-cisplatin-in-lung-cancer-cells
#2
He-Guo Jiang, Ping Chen, Jin-Yu Su, Ming Wu, Hai Qian, Yi Wang, Jian Li
It has been demonstrated that REV3, the catalytic subunit of the translesion synthesis (TLS) polymerase ζ, play an important role in DNA damage response (DDR) induced by cisplatin, and Ataxia telangietasia mutated and Rad-3-related (ATR) knase is a central player in activating cell cycle checkpoint, stabilizing replication forks, regulating DDR, and promoting repair of DNA damage caused by cisplatin. Cancer cells deficient in either one of REV3 and ATR are more sensitive to cisplatin. However, whether co-inhibition of REV3 and ATR can further increase sensitivity of non-small cell lung cancer (NSCLC) cells to cisplatin is not clear...
January 11, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28073589/mechanisms-of-oncogene-induced-genomic-instability
#3
Simona Graziano, Susana Gonzalo
Activating mutations in oncogenes promote uncontrolled proliferation and malignant transformation. Approximately 30% of human cancers carry mutations in the RAS oncogene. Paradoxically, expression of mutant constitutively active Ras protein in primary human cells results in a premature proliferation arrest known as oncogene-induced senescence (OIS). This is more commonly observed in human pre-neoplasia than in neoplastic lesions, and is considered a tumor suppressor mechanism. Senescent cells are still metabolically active but in a status of cell cycle arrest characterized by specific morphological and physiological features that distinguish them from both proliferating cells, and cells growth-arrested by other means...
November 24, 2016: Biophysical Chemistry
https://www.readbyqxmd.com/read/28058462/imaging-the-dna-damage-response-with-pet-and-spect
#4
REVIEW
James C Knight, Sofia Koustoulidou, Bart Cornelissen
DNA integrity is constantly challenged by endogenous and exogenous factors that can alter the DNA sequence, leading to mutagenesis, aberrant transcriptional activity, and cytotoxicity. Left unrepaired, damaged DNA can ultimately lead to the development of cancer. To overcome this threat, a series of complex mechanisms collectively known as the DNA damage response (DDR) are able to detect the various types of DNA damage that can occur and stimulate the appropriate repair process. Each DNA damage repair pathway leads to the recruitment, upregulation, or activation of specific proteins within the nucleus, which, in some cases, can represent attractive targets for molecular imaging...
January 5, 2017: European Journal of Nuclear Medicine and Molecular Imaging
https://www.readbyqxmd.com/read/28046999/su-f-sps-08-measuring-the-interaction-of-ddr-cell-receptors-and-extracellular-matrix-collagen-in-prostate-cells
#5
J Dong, A Sarkar, A Suhail, R Fridman, P Hoffmann
PURPOSE: Discoidin domain receptors (DDR) have recently been recognized as important players in cancer progression. DDRs are cell receptors that interact with collagen, an extracellular matrix (ECM) protein. However the detailed mechanism of their interaction is unclear. Here we attempted to examine their interaction in terms of structural (surface topography), mechanical (rupture force), and kinetic (binding probability) information on the single molecular scale with the use of atomic force microscopy (AFM)...
June 2016: Medical Physics
https://www.readbyqxmd.com/read/28041875/snev-hprp19-hpso4-regulates-adipogenesis-of-human-adipose-stromal-cells
#6
Abdulhameed Khan, Hanna Dellago, Lucia Terlecki-Zaniewicz, Michael Karbiener, Sylvia Weilner, Florian Hildner, Viktoria Steininger, Christian Gabriel, Christoph Mück, Pidder Jansen-Dürr, Ara Hacobian, Marcel Scheideler, Regina Grillari-Voglauer, Markus Schosserer, Johannes Grillari
Aging is accompanied by loss of subcutaneous adipose tissue. This may be due to reduced differentiation capacity or deficiency in DNA damage repair (DDR) factors. Here we investigated the role of SNEV(hPrp19/hPso4), which was implicated in DDR and senescence evasion, in adipogenic differentiation of human adipose stromal cells (hASCs). We showed that SNEV is induced during adipogenesis and localized both in the nucleus and in the cytoplasm. Knockdown of SNEV perturbed adipogenic differentiation and led to accumulation of DNA damage in hASCs upon oxidative stress...
January 10, 2017: Stem Cell Reports
https://www.readbyqxmd.com/read/28035971/aflatoxin-b%C3%A2-induced-developmental-and-dna-damage-in-caenorhabditis-elegans
#7
Wei-Hong Feng, Kathy S Xue, Lili Tang, Phillip L Williams, Jia-Sheng Wang
Aflatoxin B₁ (AFB₁) is a ubiquitous mycotoxin produced by toxicogenic Aspergillus species. AFB₁ has been reported to cause serious adverse health effects, such as cancers and abnormal development and reproduction, in animals and humans. AFB₁ is also a potent genotoxic mutagen that causes DNA damage in vitro and in vivo. However, the link between DNA damage and abnormal development and reproduction is unclear. To address this issue, we examined the DNA damage, germline apoptosis, growth, and reproductive toxicity following exposure to AFB₁, using Caenorhabditis elegans as a study model...
December 26, 2016: Toxins
https://www.readbyqxmd.com/read/28035404/arrb1-enhances-the-chemosensitivity-of-lung-cancer-through-the-mediation-of-dna-damage-response
#8
Hongchang Shen, Liguang Wang, Jiangang Zhang, Wei Dong, Tiehong Zhang, Yang Ni, Hongxin Cao, Kai Wang, Yun Li, Yibing Wang, Jiajun Du
ARRB1 (also known as β-arrestin-1) serves as a multifunctional adaptor contributing to the regulation of signaling pathways. ARRB1 may be involved in DNA damage accumulation; however the underlying mechanism involved is unclear. In the present study, non-small cell lung cancer (NSCLC) cell lines (H520 and SK-MES-1) were transfected with ARRB1 plasmids or small interfering ribonucleic acid (siRNA) and received treatment with DNA-damaging agents (cisplatin and etoposide). A mouse xenograft model was used to assess the impact of ARRB1 on the efficacy of cisplatin in vivo...
February 2017: Oncology Reports
https://www.readbyqxmd.com/read/28034453/dna-damage-repair-in-breast-cancer-and-its-therapeutic-implications
#9
REVIEW
Reem Ali, Emad A Rakha, Srinivasan Madhusudan, Helen E Bryant
The DNA damage response (DDR) involves the activation of numerous cellular activities that repair DNA lesions and maintain genomic integrity, and is critical in preventing tumorigenesis. Inherited or acquired mutations in specific genes involved in the DNA damage response, for example the breast cancer susceptibility genes 1/2 (BRCA1/2), phosphatase and tensin homolog (PTEN) and P53 are associated with various subtypes of breast cancer. Such changes can render breast cancer cells particularly sensitive to specific DNA damage response inhibitors, for example BRCA1/2 germline mutated cells are sensitive to poly (ADP-ribose) polymerase (PARP) inhibitors...
December 26, 2016: Pathology
https://www.readbyqxmd.com/read/28032863/short-term-inhibition-of-tert-induces-telomere-length-independent-cell-cycle-arrest-and-apoptotic-response-in-ebv-immortalized-and-transformed-b-cells
#10
Andrea Celeghin, Silvia Giunco, Riccardo Freguja, Manuela Zangrossi, Silvia Nalio, Riccardo Dolcetti, Anita De Rossi
Besides its canonical role in stabilizing telomeres, telomerase reverse transcriptase (TERT) may promote tumorigenesis through extra-telomeric functions. The possible therapeutic effects of BIBR1532 (BIBR), a powerful TERT inhibitor, have been evaluated in different cellular backgrounds, but no data are currently available regarding Epstein-Barr virus (EBV)-driven B-cell malignancies. Our aim was to characterize the biological effects of TERT inhibition by BIBR on EBV-immortalized lymphoblastoid cell lines (LCLs) and fully transformed Burkitt's lymphoma (BL) cell lines...
December 29, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/28031537/activation-of-atr-chk1-pathway-facilitates-ebv-mediated-transformation-of-primary-tonsillar-b-cells
#11
Vanessa Mordasini, Seigo Ueda, Roberta Aslandogmus, Christoph Berger, Claudine Gysin, Daniela Hühn, Alessandro A Sartori, Michele Bernasconi, David Nadal
Primary infection of the immunocompromised host with the oncovirus Epstein-Barr virus (EBV) that targets mainly B-cells is associated with an increased risk for EBV-associated tumors. The early events subsequent to primary infection with potential for B-cell transformation are poorly studied. Here, we modeled in vitro the primary infection by using B-cells isolated from tonsils, the portal of entry of EBV, since species specificity of EBV hampers modeling in experimental animals. Increasing evidence indicates that the host DNA damage response (DDR) can influence and be influenced by EBV infection...
December 23, 2016: Oncotarget
https://www.readbyqxmd.com/read/28028232/two-independent-s-phase-checkpoints-regulate-appressorium-mediated-plant-infection-by-the-rice-blast-fungus-magnaporthe-oryzae
#12
Míriam Osés-Ruiz, Wasin Sakulkoo, George R Littlejohn, Magdalena Martin-Urdiroz, Nicholas J Talbot
To cause rice blast disease, the fungal pathogen Magnaporthe oryzae develops a specialized infection structure called an appressorium. This dome-shaped, melanin-pigmented cell generates enormous turgor and applies physical force to rupture the rice leaf cuticle using a rigid penetration peg. Appressorium-mediated infection requires septin-dependent reorientation of the F-actin cytoskeleton at the base of the infection cell, which organizes polarity determinants necessary for plant cell invasion. Here, we show that plant infection by M...
January 10, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28028224/ape2-zf-grf-facilitates-3-5-resection-of-dna-damage-following-oxidative-stress
#13
Bret D Wallace, Zachary Berman, Geoffrey A Mueller, Yunfeng Lin, Timothy Chang, Sara N Andres, Jessica L Wojtaszek, Eugene F DeRose, C Denise Appel, Robert E London, Shan Yan, R Scott Williams
The Xenopus laevis APE2 (apurinic/apyrimidinic endonuclease 2) nuclease participates in 3'-5' nucleolytic resection of oxidative DNA damage and activation of the ATR-Chk1 DNA damage response (DDR) pathway via ill-defined mechanisms. Here we report that APE2 resection activity is regulated by DNA interactions in its Zf-GRF domain, a region sharing high homology with DDR proteins Topoisomerase 3α (TOP3α) and NEIL3 (Nei-like DNA glycosylase 3), as well as transcription and RNA regulatory proteins, such as TTF2 (transcription termination factor 2), TFIIS, and RPB9...
December 27, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28027876/ercc2-xpd-lys751gln-alter-dna-repair-efficiency-of-platinum-induced-dna-damage-through-p53-pathway
#14
Guopei Zhang, Yangyang Guan, Yuejiao Zhao, Tahar van der Straaten, Sha Xiao, Ping Xue, Guolian Zhu, Qiufang Liu, Yuan Cai, Cuihong Jin, Jinghua Yang, Shengwen Wu, Xiaobo Lu
Platinum-based treatment causes Pt-DNA adducts which lead to cell death. The platinum-induced DNA damage is recognized and repaired by the nucleotide excision repair (NER) system of which ERCC2/XPD is a critical enzyme. Single nucleotide polymorphisms in ERCC2/XPD have been found to be associated with platinum resistance. The aim of the present study was to investigate whether ERCC2/XPD Lys751Gln (rs13181) polymorphism is causally related to DNA repair capacity of platinum-induced DNA damage. First, cDNA clones expressing different genotypes of the polymorphism was transfected to an ERCC2/XPD defective CHO cell line (UV5)...
December 24, 2016: Chemico-biological Interactions
https://www.readbyqxmd.com/read/28027003/lzap-is-a-novel-wip1-binding-partner-and-positive-regulator-of-its-phosphatase-activity-in-vitro
#15
J Jacob Wamsley, Natalia Issaeva, Hanbing An, Xinyuan Lu, Lawrence A Donehower, Wendell G Yarbrough
The phosphatase Wip1 attenuates the DNA damage response (DDR) by removing phosphorylation marks from a number of DDR proteins (p53, MDM2, Chk1/2, p38). Wip1 also dephosphorylates and inactivates RelA. Notably, LZAP, a putative tumor suppressor, has been linked to dephosphorylation of several of these substrates, including RelA, p38, Chk1, and Chk2. LZAP has no known catalytic activity or functional motifs, suggesting that it exerts its effects through interaction with other proteins. Here we show that LZAP binds Wip1 and stimulates its phosphatase activity...
December 27, 2016: Cell Cycle
https://www.readbyqxmd.com/read/28003236/targeting-dna-repair-in-cancer-beyond-parp-inhibitors
#16
REVIEW
Jessica S Brown, Brent O'Carrigan, Stephen P Jackson, Timothy A Yap
: Germline aberrations in critical DNA-repair and DNA damage-response (DDR) genes cause cancer predisposition, whereas various tumors harbor somatic mutations causing defective DDR/DNA repair. The concept of synthetic lethality can be exploited in such malignancies, as exemplified by approval of poly(ADP-ribose) polymerase inhibitors for treating BRCA1/2-mutated ovarian cancers. Herein, we detail how cellular DDR processes engage various proteins that sense DNA damage, initiate signaling pathways to promote cell-cycle checkpoint activation, trigger apoptosis, and coordinate DNA repair...
January 2017: Cancer Discovery
https://www.readbyqxmd.com/read/27999209/s4s8-rpa-phosphorylation-as-an-indicator-of-cancer-progression-in-oral-squamous-cell-carcinomas
#17
Jeff Rector, Sasha Kapil, Kelly J Treude, Phyllis Kumm, Jason G Glanzer, Brendan M Byrne, Shengqin Liu, Lynette M Smith, Dominick J DiMaio, Peter Giannini, Russell B Smith, Greg G Oakley
Oral cancers are easily accessible compared to many other cancers. Nevertheless, oral cancer is often diagnosed late, resulting in a poor prognosis. Most oral cancers are squamous cell carcinomas that predominantly develop from cell hyperplasias and dysplasias. DNA damage is induced in these tissues directly or indirectly in response to oncogene-induced deregulation of cellular proliferation. Consequently, a DNA Damage response (DDR) and a cell cycle checkpoint is activated. As dysplasia transitions to cancer, proteins involved in DNA damage and checkpoint signaling are mutated or silenced decreasing cell death while increasing genomic instability and allowing continued tumor progression...
December 16, 2016: Oncotarget
https://www.readbyqxmd.com/read/27999166/the-cytolethal-distending-toxin-produced-by-nontyphoidal-salmonella-serotypes-javiana-montevideo-oranienburg-and-mississippi-induces-dna-damage-in-a-manner-similar-to-that-of-serotype-typhi
#18
Rachel A Miller, Martin Wiedmann
: Select nontyphoidal Salmonella enterica (NTS) serotypes were recently found to encode the Salmonella cytolethal distending toxin (S-CDT), an important virulence factor for serotype Typhi, the causative agent of typhoid fever. Using a PCR-based assay, we determined that among 21 NTS serotypes causing the majority of food-borne salmonellosis cases in the United States, genes encoding S-CDT are conserved in isolates representing serotypes Javiana, Montevideo, and Oranienburg but that among serotype Mississippi isolates, the presence of S-CDT-encoding genes is clade associated...
December 20, 2016: MBio
https://www.readbyqxmd.com/read/27996159/persistent-phosphorylation-at-specific-h3-serine-residues-involved-in-chemical-carcinogen-induced-cell-transformation
#19
Xiaonian Zhu, Daochuan Li, Zhengbao Zhang, Wei Zhu, Wenxue Li, Jian Zhao, Xiumei Xing, Zhini He, Shan Wang, Fangping Wang, Lu Ma, Qing Bai, Xiaowen Zeng, Jie Li, Chen Gao, Yongmei Xiao, Qing Wang, Liping Chen, Wen Chen
Identification of aberrant histone H3 phosphorylation during chemical carcinogenesis will lead to a better understanding of the substantial roles of histone modifications in cancer development. To explore whether aberrant H3 phosphorylation contributes to chemical carcinogenesis, we examined the dynamic changes of H3 phosphorylation at various residues in chemical carcinogen-induced transformed human cells and human cancers. We found that histone H3 phosphorylation at Ser10 (p-H3S10) and Ser28 (p-H3S28) were up-regulated by 1...
December 20, 2016: Molecular Carcinogenesis
https://www.readbyqxmd.com/read/27991914/the-spliceosome-u2-snrnp-factors-promote-genome-stability-through-distinct-mechanisms-transcription-of-repair-factors-and-r-loop-processing
#20
M Tanikawa, K Sanjiv, T Helleday, P Herr, O Mortusewicz
Recent whole-exome sequencing of malignancies have detected recurrent somatic mutations in U2 small nuclear ribonucleoprotein complex (snRNP) components of the spliceosome. These factors have also been identified as novel players in the DNA-damage response (DDR) in several genome-wide screens and proteomic analysis. Although accumulating evidence implies that the spliceosome has an important role in genome stability and is an emerging hallmark of cancer, its precise role in DNA repair still remains elusive...
December 19, 2016: Oncogenesis
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