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3. A two-step mechanism for TRF2-mediated chromosome-end protection

Author

Okamoto, Keiji, Bartocci, Cristina, Ouzounov, Iliana, Diedrich, Jolene K., Yates, III, John R., and Denchi, Eros Lazzerini

Subjects
Binding proteins -- Observations, DNA damage -- Research, Telomeres -- Properties, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Mammalian telomeres repress DNA-damage activation at natural chromosome ends by recruiting specific inhibitors of the DNA-damage machinery that form a protective complex termed shelterin. Within this complex, TRF2 (also known [...]

Published
2013
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5. Genome-wide Association Analysis in Humans Links Nucleotide Metabolism to Leukocyte Telomere Length

Author

Li, Chen, primary, Stoma, Svetlana, additional, Lotta, Luca A., additional, Warner, Sophie, additional, Albrecht, Eva, additional, Allione, Alessandra, additional, Arp, Pascal P., additional, Broer, Linda, additional, Buxton, Jessica L., additional, Da Silva Couto Alves, Alexessander, additional, Deelen, Joris, additional, Fedko, Iryna O., additional, Gordon, Scott D., additional, Jiang, Tao, additional, Karlsson, Robert, additional, Kerrison, Nicola, additional, Loe, Taylor K., additional, Mangino, Massimo, additional, Milaneschi, Yuri, additional, Miraglio, Benjamin, additional, Pervjakova, Natalia, additional, Russo, Alessia, additional, Surakka, Ida, additional, van der Spek, Ashley, additional, Verhoeven, Josine E., additional, Amin, Najaf, additional, Beekman, Marian, additional, Blakemore, Alexandra I., additional, Canzian, Federico, additional, Hamby, Stephen E., additional, Hottenga, Jouke-Jan, additional, Jones, Peter D., additional, Jousilahti, Pekka, additional, Mägi, Reedik, additional, Medland, Sarah E., additional, Montgomery, Grant W., additional, Nyholt, Dale R., additional, Perola, Markus, additional, Pietiläinen, Kirsi H., additional, Salomaa, Veikko, additional, Sillanpää, Elina, additional, Suchiman, H. Eka, additional, van Heemst, Diana, additional, Willemsen, Gonneke, additional, Agudo, Antonio, additional, Boeing, Heiner, additional, Boomsma, Dorret I., additional, Chirlaque, Maria-Dolores, additional, Fagherazzi, Guy, additional, Ferrari, Pietro, additional, Franks, Paul, additional, Gieger, Christian, additional, Eriksson, Johan Gunnar, additional, Gunter, Marc, additional, Hägg, Sara, additional, Hovatta, Iiris, additional, Imaz, Liher, additional, Kaprio, Jaakko, additional, Kaaks, Rudolf, additional, Key, Timothy, additional, Krogh, Vittorio, additional, Martin, Nicholas G., additional, Melander, Olle, additional, Metspalu, Andres, additional, Moreno, Concha, additional, Onland-Moret, N. Charlotte, additional, Nilsson, Peter, additional, Ong, Ken K., additional, Overvad, Kim, additional, Palli, Domenico, additional, Panico, Salvatore, additional, Pedersen, Nancy L., additional, Penninx, Brenda W.J. H., additional, Quirós, J. Ramón, additional, Jarvelin, Marjo Riitta, additional, Rodríguez-Barranco, Miguel, additional, Scott, Robert A., additional, Severi, Gianluca, additional, Slagboom, P. Eline, additional, Spector, Tim D., additional, Tjonneland, Anne, additional, Trichopoulou, Antonia, additional, Tumino, Rosario, additional, Uitterlinden, André G., additional, van der Schouw, Yvonne T., additional, van Duijn, Cornelia M., additional, Weiderpass, Elisabete, additional, Denchi, Eros Lazzerini, additional, Matullo, Giuseppe, additional, Butterworth, Adam S., additional, Danesh, John, additional, Samani, Nilesh J., additional, Wareham, Nicholas J., additional, Nelson, Christopher P., additional, Langenberg, Claudia, additional, and Codd, Veryan, additional

Published
2020
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8. Hepatocytes with extensive telomere deprotection and fusion remain viable and regenerate liver mass through endoreduplication

Author

Denchi, Eros Lazzerini, Celli, Giulia, and de Lange, Titia

Subjects
Chromosome replication -- Analysis, DNA damage -- Analysis, Liver cells -- Research, Telomeres -- Research, Biological sciences
Abstract

Mouse liver cells are highly resistant to extensive telomere dysfunction and the consequences of telomere dysfunction in noncycling cells are determined by using conditional deletion of the telomeric protein TRF2 in hepatocytes. The nondividing hepatocytes are found to maintain and regenerate liver function despite substantial loss of telomere integrity.

Published
2006

13. Mitotic Evolution of Plasmodium falciparum Shows a Stable Core Genome but Recombination in Antigen Families

Author

Bopp, Selina E. R., primary, Manary, Micah J., additional, Bright, A. Taylor, additional, Johnston, Geoffrey L., additional, Dharia, Neekesh V., additional, Luna, Fabio L., additional, McCormack, Susan, additional, Plouffe, David, additional, McNamara, Case W., additional, Walker, John R., additional, Fidock, David A., additional, Denchi, Eros Lazzerini, additional, and Winzeler, Elizabeth A., additional

Published
2013
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24. Nucleophosmin Is Required for DNA Integrity and p19Arf Protein Stability.

Author

Colombo, Emanuela, Bonetti, Paola, Denchi, Eros Lazzerini, Martinelli, Paola, Zamponi, Raffaella, Marine, Jean-Christophe, Helin, Kristian, Falini, Brunangelo, and Pelicci, Pier Giuseppe

Subjects
PHOSPHOPROTEINS, P53 protein, RIBOSE, CELL proliferation, DNA, TUMOR suppressor proteins, PROTEINS
Abstract

Nucleophosmin (NPM) is a nucleolar phosphoprotein that binds the tumor suppressors p53 and p19Arf and is thought to be indispensable for ribogenesis, cell proliferation, and survival after DNA damage. The NPM gene is the most frequent target of genetic alterations in leukemias and lymphomas, though its role in tumorigenesis is unknown. We report here the first characterization of a mouse NPM knockout strain. Lack of NPM expression results in accumulation of DNA damage, activation of p53, widespread apoptosis, and mid-stage embryonic lethality. Fibroblasts explanted from null embryos fail to grow and rapidly acquire a senescent phenotype. Transfer of the NPM mutation into a p53-null background rescued apoptosis in vivo and fibroblast proliferation in vitro. Cells null for both p53 and NPM grow faster than control cells and are more susceptible to transformation by activated oncogenes, such as mutated Ras or overexpressed Myc. In the absence of NPM, Arf protein is excluded from nucleoli and is markedly less stable. Our data demonstrate that NPM regulates DNA integrity and, through Aft, inhibits cell proliferation and are consistent with a putative tumor-suppressive function of NPM. [ABSTRACT FROM AUTHOR]

Published
2005
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25. DUB-resistant ubiquitin to survey ubiquitination switches in mammalian cells.

Author

Békés M, Okamoto K, Crist SB, Jones MJ, Chapman JR, Brasher BB, Melandri FD, Ueberheide BM, Denchi EL, and Huang TT

Subjects
Amino Acid Sequence, Cell Line, Tumor, DNA Damage, HEK293 Cells, Humans, Molecular Sequence Data, Proliferating Cell Nuclear Antigen metabolism, Ubiquitin genetics, Ubiquitin-Specific Proteases metabolism, Ubiquitination, Ubiquitin metabolism
Abstract

The ubiquitin-modification status of proteins in cells is highly dynamic and maintained by specific ligation machineries (E3 ligases) that tag proteins with ubiquitin or by deubiquitinating enzymes (DUBs) that remove the ubiquitin tag. The development of tools that offset this balance is critical in characterizing signaling pathways that utilize such ubiquitination switches. Herein, we generated a DUB-resistant ubiquitin mutant that is recalcitrant to cleavage by various families of DUBs both in vitro and in mammalian cells. As a proof-of-principle experiment, ectopic expression of the uncleavable ubiquitin stabilized monoubiquitinated PCNA in the absence of DNA damage and also revealed a defect in the clearance of the DNA damage response at unprotected telomeres. Importantly, a proteomic survey using the uncleavable ubiquitin identified ubiquitinated substrates, validating the DUB-resistant ubiquitin expression system as a valuable tool for interrogating cell signaling pathways., (Copyright © 2013 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2013
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