Zobrazeno 1 - 10
of 26
pro vyhledávání: '"Robert J.D. Reid"'
Autor:
Beatrice Rondinelli, Giulia Giacomini, Sandra Piquet, Odile Chevallier, Juliette Dabin, Siau-Kun Bai, Byungjin Kim, Robert Siddaway, Brian Raught, Etienne Coyaud, Chun-Min Shan, Robert J.D. Reid, Takenori Toda, Rodney Rothstein, Therese Wilhelm, Viviana Barra, Alexander Crane, Frank Dubois, Pratiti Bandopadhayay, Rameen Beroukhim, Valeria Naim, Songtao Jia, Cynthia Hawkins, Sophie E. Polo
SummaryPediatric high-grade gliomas (pHGG) are devastating and incurable brain tumors with recurrent mutations in histone H3.3. These mutations promote oncogenesis by dysregulating gene expression through alterations of histone modifications. We iden
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::40463c61815d585524069a95554c8883
https://doi.org/10.1101/2022.09.29.510093
https://doi.org/10.1101/2022.09.29.510093
Publikováno v:
Nucleic Acids Research
The postreplication repair gene, HLTF, is often amplified and overexpressed in cancer. Here we model HLTF dysregulation through the functionally conserved Saccharomyces cerevisiae ortholog, RAD5. Genetic interaction profiling and landscape enrichment
Autor:
Lodewyk F. A. Wessels, René Bernards, Robert J.D. Reid, John C. Dittmar, Evert Bosdriesz, Cor Lieftink, Roderick L. Beijersbergen, Sake van Wageningen, Rodney Rothstein, Tonći Šuštić
Publikováno v:
Genome Medicine
Šuštić, T, van Wageningen, S, Bosdriesz, E, Reid, R J D, Dittmar, J, Lieftink, C, Beijersbergen, R L, Wessels, L F A, Rothstein, R & Bernards, R 2018, ' A role for the unfolded protein response stress sensor ERN1 in regulating the response to MEK inhibitors in KRAS mutant colon cancers ', Genome Medicine, vol. 10, no. 1, 90, pp. 90 . https://doi.org/10.1186/s13073-018-0600-z
Genome Medicine, 10(1):90. BioMed Central
Genome Medicine, Vol 10, Iss 1, Pp 1-13 (2018)
Šuštić, T, van Wageningen, S, Bosdriesz, E, Reid, R J D, Dittmar, J, Lieftink, C, Beijersbergen, R L, Wessels, L F A, Rothstein, R & Bernards, R 2018, ' A role for the unfolded protein response stress sensor ERN1 in regulating the response to MEK inhibitors in KRAS mutant colon cancers ', Genome Medicine, vol. 10, no. 1, 90, pp. 90 . https://doi.org/10.1186/s13073-018-0600-z
Genome Medicine, 10(1):90. BioMed Central
Genome Medicine, Vol 10, Iss 1, Pp 1-13 (2018)
BackgroundMutations inKRASare frequent in human cancer, yet effective targeted therapeutics for these cancers are still lacking. Attempts to drug the MEK kinases downstream of KRAS have had limited success in clinical trials. Understanding the specif
Autor:
Eric E. Bryant, John C. Dittmar, Rodney Rothstein, Xing Du, Matthew Maurer, Robert J.D. Reid, Vinayak Rayannavar, Ivana Sunjevaric
Publikováno v:
Genetics
The CKS1B gene located on chromosome 1q21 is frequently amplified in breast, lung, and liver cancers. CKS1B codes for a conserved regulatory subunit of cyclin–CDK complexes that function at multiple stages of cell cycle progression. We used a high
Autor:
Eugene Futai, Erik L. Snapp, Randy Schekman, Robert J.D. Reid, Rodney Rothstein, Susan Hamamoto, Jennifer G. D’Arcangelo, Silvere Pagant, John C. Dittmar, Leslie Kung, Roy Buchanan, Elizabeth A. Miller
Publikováno v:
The EMBO Journal. 31:1014-1027
Vesicle budding from the endoplasmic reticulum (ER) employs a cycle of GTP binding and hydrolysis to regulate assembly of the COPII coat. We have identified a novel mutation (sec24-m11) in the cargo-binding subunit, Sec24p, that specifically impacts
Autor:
Kara A. Bernstein, Rodney Rothstein, Robert J.D. Reid, Ivana Sunjevaric, Kimberly Demuth, Rebecca C. Burgess
Publikováno v:
Molecular Biology of the Cell
The Shu complex, which contains RAD51 paralogues, is involved in the decision between homologous recombination and error-prone repair. A novel role for the Shu complex in DNA recombination is proposed in which the Shu complex shifts the balance of re
Autor:
Robert J.D. Reid, Adriana Antúnez de Mayolo, Michael Lisby, Uffe Hasbro Mortensen, Ivana Sunjevaric, Rodney Rothstein
Publikováno v:
DNA Repair. 9:23-32
Spontaneous mitotic recombination is a potential source of genetic changes such as loss of heterozygosity and chromosome translocations, which may lead to genetic disease. In this study we have used a rad52 hyper-recombination mutant, rad52-Y66A, to
Autor:
Robert J.D. Reid, Stefan Jentsch, Luis Aragón, Michael Lisby, Ivana Sunjevaric, Nadine Eckert-Boulet, Meik Sacher, Jordi Torres-Rosell, Giacomo De Piccoli, Rodney Rothstein
Publikováno v:
ResearcherID
Homologous recombination (HR) is crucial for maintaining genome integrity by repairing DNA double-strand breaks (DSBs) and rescuing collapsed replication forks. In contrast, uncontrolled HR can lead to chromosome translocations, loss of heterozygosit
Autor:
Hervé R. Jacquiau, Robert C.A.M. van Waardenburg, Erica S. Johnson, Hong Guo, Michael H. Woo, Robert J.D. Reid, Mary-Ann Bjornsti
Publikováno v:
Journal of Biological Chemistry. 280:23566-23575
Eukaryotic DNA topoisomerase I (Top1p) has important functions in DNA replication, transcription, and recombination. This enzyme also constitutes the cellular target of camptothecin (CPT), which induces S-phase-dependent cytotoxicity. To define cellu
Publikováno v:
Proceedings of the National Academy of Sciences of the United States of America 96 (1999): 11440–11445. doi:10.1073/pnas.96.20.11440
info:cnr-pdr/source/autori:Reid R.J.D.; Fiorani P.; Sugawara M.; Bjornsti M.-A./titolo:CDC45 and DPB11 are required for processive DNA replication and resistance to DNA topoisomerase I-mediated DNA damage/doi:10.1073%2Fpnas.96.20.11440/rivista:Proceedings of the National Academy of Sciences of the United States of America/anno:1999/pagina_da:11440/pagina_a:11445/intervallo_pagine:11440–11445/volume:96
info:cnr-pdr/source/autori:Reid R.J.D.; Fiorani P.; Sugawara M.; Bjornsti M.-A./titolo:CDC45 and DPB11 are required for processive DNA replication and resistance to DNA topoisomerase I-mediated DNA damage/doi:10.1073%2Fpnas.96.20.11440/rivista:Proceedings of the National Academy of Sciences of the United States of America/anno:1999/pagina_da:11440/pagina_a:11445/intervallo_pagine:11440–11445/volume:96
The antitumor agent camptothecin targets DNA topoisomerase I by reversibly stabilizing a covalent enzyme-DNA intermediate. The subsequent collision of DNA replication forks with these drug-enzyme-DNA complexes produces the cytotoxic DNA lesions that