keyword
MENU ▼
Read by QxMD icon Read
search

REV7

keyword
https://www.readbyqxmd.com/read/29768208/the-cst-complex-mediates-end-protection-at-double-strand-breaks-and-promotes-parp-inhibitor-sensitivity-in-brca1-deficient-cells
#1
Marco Barazas, Stefano Annunziato, Stephen J Pettitt, Inge de Krijger, Hind Ghezraoui, Stefan J Roobol, Catrin Lutz, Jessica Frankum, Fei Fei Song, Rachel Brough, Bastiaan Evers, Ewa Gogola, Jinhyuk Bhin, Marieke van de Ven, Dik C van Gent, Jacqueline J L Jacobs, Ross Chapman, Christopher J Lord, Jos Jonkers, Sven Rottenberg
Selective elimination of BRCA1-deficient cells by inhibitors of poly(ADP-ribose) polymerase (PARP) is a prime example of the concept of synthetic lethality in cancer therapy. This interaction is counteracted by the restoration of BRCA1-independent homologous recombination through loss of factors such as 53BP1, RIF1, and REV7/MAD2L2, which inhibit end resection of DNA double-strand breaks (DSBs). To identify additional factors involved in this process, we performed CRISPR/SpCas9-based loss-of-function screens and selected for factors that confer PARP inhibitor (PARPi) resistance in BRCA1-deficient cells...
May 15, 2018: Cell Reports
https://www.readbyqxmd.com/read/29748565/genome-wide-and-high-density-crispr-cas9-screens-identify-point-mutations-in-parp1-causing-parp-inhibitor-resistance
#2
Stephen J Pettitt, Dragomir B Krastev, Inger Brandsma, Amy Dréan, Feifei Song, Radoslav Aleksandrov, Maria I Harrell, Malini Menon, Rachel Brough, James Campbell, Jessica Frankum, Michael Ranes, Helen N Pemberton, Rumana Rafiq, Kerry Fenwick, Amanda Swain, Sebastian Guettler, Jung-Min Lee, Elizabeth M Swisher, Stoyno Stoynov, Kosuke Yusa, Alan Ashworth, Christopher J Lord
Although PARP inhibitors (PARPi) target homologous recombination defective tumours, drug resistance frequently emerges, often via poorly understood mechanisms. Here, using genome-wide and high-density CRISPR-Cas9 "tag-mutate-enrich" mutagenesis screens, we identify close to full-length mutant forms of PARP1 that cause in vitro and in vivo PARPi resistance. Mutations both within and outside of the PARP1 DNA-binding zinc-finger domains cause PARPi resistance and alter PARP1 trapping, as does a PARP1 mutation found in a clinical case of PARPi resistance...
May 10, 2018: Nature Communications
https://www.readbyqxmd.com/read/29697047/rev7-and-53bp1-crb2-prevent-recq-helicase-dependent-hyper-resection-of-dna-double-strand-breaks
#3
Bryan A Leland, Angela C Chen, Amy Y Zhao, Robert C Wharton, Megan C King
Poly(ADP ribose) polymerase inhibitors (PARPi) target cancer cells deficient in homology-directed repair of DNA double-strand breaks (DSBs). In preclinical models, PARPi resistance is tied to altered nucleolytic processing (resection) at the 5' ends of a DSB. For example, loss of 53BP1 or Rev7/MAD2L2/FANCV derepresses resection to drive PARPi resistance, although the mechanisms are poorly understood. Long-range resection can be catalyzed by two machineries: the exonuclease Exo1, or the combination of a RecQ helicase and Dna2...
April 26, 2018: ELife
https://www.readbyqxmd.com/read/29656893/dna-repair-network-analysis-reveals-shieldin-as-a-key-regulator-of-nhej-and-parp-inhibitor-sensitivity
#4
Rajat Gupta, Kumar Somyajit, Takeo Narita, Elina Maskey, Andre Stanlie, Magdalena Kremer, Dimitris Typas, Michael Lammers, Niels Mailand, Andre Nussenzweig, Jiri Lukas, Chunaram Choudhary
Repair of damaged DNA is essential for maintaining genome integrity and for preventing genome-instability-associated diseases, such as cancer. By combining proximity labeling with quantitative mass spectrometry, we generated high-resolution interaction neighborhood maps of the endogenously expressed DNA repair factors 53BP1, BRCA1, and MDC1. Our spatially resolved interaction maps reveal rich network intricacies, identify shared and bait-specific interaction modules, and implicate previously concealed regulators in this process...
May 3, 2018: Cell
https://www.readbyqxmd.com/read/29360267/mad2l2-inhibits-colorectal-cancer-growth-by-promoting-ncoa3-ubiquitination-and-degradation
#5
Yixin Li, Liren Li, Miao Chen, Xinfa Yu, Zhuoyu Gu, Huijuan Qiu, Ge Qin, Qian Long, Xiaoyan Fu, Tianze Liu, Wenbin Li, Wenlin Huang, Dingbo Shi, Tiebang Kang, Meihua Luo, Xiaojun Wu, Wuguo Deng
Nuclear receptor coactivator 3 (NCOA3) is a transcriptional coactivator that has elevated expression in multiple tumor types, including colorectal cancer (CRC). However, the molecular mechanisms that regulate the tumorigenic functions of NCOA3 in CRC remain largely unknown. In this study, we aimed to discover and identify the novel regulatory proteins of NCOA3 and explore their mechanisms of action. Immunoprecipitation (IP) coupled with mass spectrometry (IP-MS) analysis was used to detect, identify, and verify the proteins that interacted with NCOA3 in CRC cells...
March 2018: Molecular Oncology
https://www.readbyqxmd.com/read/28887307/dynamic-feature-of-mitotic-arrest-deficient-2-like-protein-2-mad2l2-and-structural-basis-for-its-interaction-with-chromosome-alignment-maintaining-phosphoprotein-camp
#6
Kodai Hara, Shota Taharazako, Masanori Ikeda, Hiroki Fujita, Yoshiko Mikami, Sotaro Kikuchi, Asami Hishiki, Hideshi Yokoyama, Yoshinobu Ishikawa, Shin-Ichiro Kanno, Kozo Tanaka, Hiroshi Hashimoto
Mitotic arrest deficient 2-like protein 2 (MAD2L2), also termed MAD2B or REV7, is involved in multiple cellular functions including translesion DNA synthesis (TLS), signal transduction, transcription, and mitotic events. MAD2L2 interacts with chromosome alignment-maintaining phosphoprotein (CAMP), a kinetochore-microtubule attachment protein in mitotic cells, presumably through a novel "WK" motif in CAMP. Structures of MAD2L2 in complex with binding regions of the TLS proteins REV3 and REV1 have revealed that MAD2L2 has two faces for protein-protein interactions that are regulated by its C-terminal region; however, the mechanisms underlying the MAD2L2-CAMP interaction and the mitotic role of MAD2L2 remain unknown...
October 27, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28440919/rev7-the-regulatory-subunit-of-pol%C3%AE-undergoes-uv-induced-and-cul4-dependent-degradation
#7
Audesh Bhat, Zhoushuai Qin, Guifen Wang, Wangyang Chen, Wei Xiao
In eukaryotic cells, Rev7 interacts with Rev3 and functions as a regulatory subunit of Polζ, a translesion DNA synthesis (TLS) polymerase. In addition to its role in TLS, mammalian Rev7, also known as Mad2B/Mad2L2, participates in multiple cellular activities including cell cycle progression and double-strand break repair through its interaction with several proteins. Here we show that in mammalian cells, Rev7 undergoes ubiquitin/proteasome-mediated degradation upon UV irradiation in a time-dependent manner...
June 2017: FEBS Journal
https://www.readbyqxmd.com/read/28248207/biallelic-inactivation-of-rev7-is-associated-with-fanconi-anemia
#8
Dominique Bluteau, Julien Masliah-Planchon, Connor Clairmont, Alix Rousseau, Raphael Ceccaldi, Catherine Dubois d'Enghien, Olivier Bluteau, Wendy Cuccuini, Stéphanie Gachet, Régis Peffault de Latour, Thierry Leblanc, Gérard Socié, André Baruchel, Dominique Stoppa-Lyonnet, Alan D D'Andrea, Jean Soulier
No abstract text is available yet for this article.
March 1, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27760710/recent-discoveries-in-the-molecular-pathogenesis-of-the-inherited-bone-marrow-failure-syndrome-fanconi-anemia
#9
REVIEW
Nicholas E Mamrak, Akiko Shimamura, Niall G Howlett
Fanconi anemia (FA) is a rare autosomal and X-linked genetic disease characterized by congenital abnormalities, progressive bone marrow failure (BMF), and increased cancer risk during early adulthood. The median lifespan for FA patients is approximately 33years. The proteins encoded by the FA genes function together in the FA-BRCA pathway to repair DNA damage and to maintain genome stability. Within the past two years, five new FA genes have been identified-RAD51/FANCR, BRCA1/FANCS, UBE2T/FANCT, XRCC2/FANCU, and REV7/FANCV-bringing the total number of disease-causing genes to 21...
May 2017: Blood Reviews
https://www.readbyqxmd.com/read/27712588/knockdown-of-rev7-inhibits-breast-cancer-cell-migration-and-invasion
#10
Liu Feng, Wang Wei, Zhang Heng, Han Yantao, Wang Chunbo
REV7 (also known as MAD2L2) is a multifunctional protein involved in DNA damage tolerance, cell cycle regulation, gene expression, and carcinogenesis. Although its expression is reportedly associated with poor prognosis in several kinds of human cancers, the significance of REV7 expression in breast malignancies is unclear. In this study, REV7 was found to be increased in breast cancer. We found that knockdown of REV7 inhibited the migration, invasion, and epithelial-mesenchymal transition (EMT) of breast cancer cells...
2016: Oncology Research
https://www.readbyqxmd.com/read/27500492/biallelic-inactivation-of-rev7-is-associated-with-fanconi-anemia
#11
Dominique Bluteau, Julien Masliah-Planchon, Connor Clairmont, Alix Rousseau, Raphael Ceccaldi, Catherine Dubois d'Enghien, Olivier Bluteau, Wendy Cuccuini, Stéphanie Gachet, Régis Peffault de Latour, Thierry Leblanc, Gérard Socié, André Baruchel, Dominique Stoppa-Lyonnet, Alan D D'Andrea, Jean Soulier
Fanconi anemia (FA) is a recessive genetic disease characterized by congenital abnormalities, chromosome instability, progressive bone marrow failure (BMF), and a strong predisposition to cancer. Twenty FA genes have been identified, and the FANC proteins they encode cooperate in a common pathway that regulates DNA crosslink repair and replication fork stability. We identified a child with severe BMF who harbored biallelic inactivating mutations of the translesion DNA synthesis (TLS) gene REV7 (also known as MAD2L2), which encodes the mutant REV7 protein REV7-V85E...
September 1, 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27448776/identification-of-the-first-small-molecule-inhibitor-of-the-rev7-dna-repair-protein-interaction
#12
Marcelo L Actis, Nigus D Ambaye, Benjamin J Evison, Youming Shao, Murugendra Vanarotti, Akira Inoue, Ezelle T McDonald, Sotaro Kikuchi, Richard Heath, Kodai Hara, Hiroshi Hashimoto, Naoaki Fujii
DNA interstrand crosslink (ICL) repair (ICLR) has been implicated in the resistance of cancer cells to ICL-inducing chemotherapeutic agents. Despite the clinical significance of ICL-inducing chemotherapy, few studies have focused on developing small-molecule inhibitors for ICLR. The mammalian DNA polymerase ζ, which comprises the catalytic subunit REV3L and the non-catalytic subunit REV7, is essential for ICLR. To identify small-molecule compounds that are mechanistically capable of inhibiting ICLR by targeting REV7, high-throughput screening and structure-activity relationship (SAR) analysis were performed...
September 15, 2016: Bioorganic & Medicinal Chemistry
https://www.readbyqxmd.com/read/26987799/dna-damage-signalling-barrier-oxidative-stress-and-treatment-relevant-dna-repair-factor-alterations-during-progression-of-human-prostate-cancer
#13
Daniela Kurfurstova, Jirina Bartkova, Radek Vrtel, Alena Mickova, Alena Burdova, Dusana Majera, Martin Mistrik, Milan Kral, Frederic R Santer, Jan Bouchal, Jiri Bartek
The DNA damage checkpoints provide an anti-cancer barrier in diverse tumour types, however this concept has remained unexplored in prostate cancer (CaP). Furthermore, targeting DNA repair defects by PARP1 inhibitors (PARPi) as a cancer treatment strategy is emerging yet requires suitable predictive biomarkers. To address these issues, we performed immunohistochemical analysis of multiple markers of DNA damage signalling, oxidative stress, DNA repair and cell cycle control pathways during progression of human prostate disease from benign hyperplasia, through intraepithelial neoplasia to CaP, complemented by genetic analyses of TMPRSS2-ERG rearrangement and NQO1, an anti-oxidant factor and p53 protector...
June 2016: Molecular Oncology
https://www.readbyqxmd.com/read/26982350/interaction-between-the-rev1-c-terminal-domain-and-the-pold3-subunit-of-pol%C3%AE-suggests-a-mechanism-of-polymerase-exchange-upon-rev1-pol%C3%AE-dependent-translesion-synthesis
#14
Yulia Pustovalova, Mariana T Q Magalhães, Sanjay D'Souza, Alessandro A Rizzo, George Korza, Graham C Walker, Dmitry M Korzhnev
Translesion synthesis (TLS) is a mutagenic branch of cellular DNA damage tolerance that enables bypass replication over DNA lesions carried out by specialized low-fidelity DNA polymerases. The replicative bypass of most types of DNA damage is performed in a two-step process of Rev1/Polζ-dependent TLS. In the first step, a Y-family TLS enzyme, typically Polη, Polι, or Polκ, inserts a nucleotide across a DNA lesion. In the second step, a four-subunit B-family DNA polymerase Polζ (Rev3/Rev7/PolD2/PolD3 complex) extends the distorted DNA primer-template...
April 5, 2016: Biochemistry
https://www.readbyqxmd.com/read/26748828/targeting-brca1-and-brca2-deficiencies-with-g-quadruplex-interacting-compounds
#15
Jutta Zimmer, Eliana M C Tacconi, Cecilia Folio, Sophie Badie, Manuela Porru, Kerstin Klare, Manuela Tumiati, Enni Markkanen, Swagata Halder, Anderson Ryan, Stephen P Jackson, Kristijan Ramadan, Sergey G Kuznetsov, Annamaria Biroccio, Julian E Sale, Madalena Tarsounas
G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers. Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks. We have previously shown that HR facilitates telomere replication. Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR. Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability...
February 4, 2016: Molecular Cell
https://www.readbyqxmd.com/read/26697843/rev7-mad2b-plays-a-critical-role-in-the-assembly-of-a-functional-mitotic-spindle
#16
Audesh Bhat, Zhaojia Wu, Veronica M Maher, J Justin McCormick, Wei Xiao
The spindle assembly checkpoint (SAC) acts as a guardian against cellular threats that may lead to chromosomal missegregation and aneuploidy. Mad2, an anaphase-promoting complex/cyclosome-Cdc20 (APC/C(Cdc20)) inhibitor, has an additional homolog in mammals known as Mad2B, Mad2L2 or Rev7. Apart from its role in Polζ-mediated translesion DNA synthesis and double-strand break repair, Rev7 is also believed to inhibit APC/C by negatively regulating Cdh1. Here we report yet another function of Rev7 in cultured human cells...
2015: Cell Cycle
https://www.readbyqxmd.com/read/26449786/high-expression-of-rev7-is-an-independent-prognostic-indicator-in-patients-with-diffuse-large-b-cell-lymphoma-treated-with-rituximab
#17
Sosei Okina, Nobuyuki Yanagisawa, Maki Yokoyama, Yasutaka Sakurai, Yoshiko Numata, Atsuko Umezawa, Masaaki Higashihara, Yoshiki Murakumo
REV7 is a multifunctional protein involved in DNA damage tolerance, cell-cycle regulation, gene expression, and carcinogenesis. Although its expression is reportedly associated with poor prognosis in human solid tissue cancers, the significance of REV7 expression in hematopoietic malignancies is unclear. This study evaluated the prognostic significance of REV7 expression in patients with diffuse large B-cell lymphoma (DLBCL) treated with rituximab-combined chemotherapy. Using immunohistochemistry, we analyzed 83 specimens of de novo DLBCL [38 germinal center B-cell-like (GCB) and 45 non-GCB DLBCLs] treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone for REV7 expression...
December 2015: International Journal of Hematology
https://www.readbyqxmd.com/read/26299944/structure-of-the-human-atg13-atg101-horma-heterodimer-an-interaction-hub-within-the-ulk1-complex
#18
Shiqian Qi, Do Jin Kim, Goran Stjepanovic, James H Hurley
The ULK1 complex, consisting of the ULK1 protein kinase itself, FIP200, Atg13, and Atg101, controls the initiation of autophagy in animals. We determined the structure of the complex of the human Atg13 HORMA (Hop1, Rev7, Mad2) domain in complex with the full-length HORMA domain-only protein Atg101. The two HORMA domains assemble with an architecture conserved in the Mad2 conformational heterodimer and the S. pombe Atg13-Atg101 HORMA complex. The WF finger motif that is essential for function in human Atg101 is sequestered in a hydrophobic pocket, suggesting that the exposure of this motif is regulated...
October 6, 2015: Structure
https://www.readbyqxmd.com/read/26278154/pol-%C3%AE-%C3%A2-polymorphisms-are-associated-with-platinum-based-chemotherapy-response-and-side-effects-among-non-small-cell-lung-cancer-patients
#19
J Ye, T Chu, R Li, Y Niu, B Jin, J Xia, M Shao, B Han
Lung cancer is the greatest contributor to tumor-derived death. Traditionally, platinum-based chemotherapies are the primary treatment for most patients. However, intrinsic drug resistance and side effects limit the efficacy of platinum-based chemotherapies. Previous studies demonstrated that Pol ζ can modulate cellular sensitivity to chemotherapy. The primary aim of this study was to investigate the potential role of the polymorphism of Pol ζ in platinum-based chemotherapy tolerance and side effects. A total of 663 patients who were newly histologically diagnosed with advanced NSCLC were enrolled...
2015: Neoplasma
https://www.readbyqxmd.com/read/26147350/the-protein-level-of-rev1-a-tls-polymerase-in-fission-yeast-is-strictly-regulated-during-the-cell-cycle-and-after-dna-damage
#20
Masashi Uchiyama, Junko Terunuma, Fumio Hanaoka
Translesion DNA synthesis provides an alternative DNA replication mechanism when template DNA is damaged. In fission yeast, Eso1 (polη), Kpa1/DinB (polκ), Rev1, and Polζ (a complex of Rev3 and Rev7) have been identified as translesion synthesis polymerases. The enzymatic characteristics and protein-protein interactions of these polymerases have been intensively characterized; however, how these proteins are regulated during the cell cycle remains unclear. Therefore, we examined the cell cycle oscillation of translesion polymerases...
2015: PloS One
keyword
keyword
120221
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"