[{"oa_version":"None","date_created":"2022-03-21T07:16:12Z","date_updated":"2022-06-21T11:51:58Z","edition":"1","author":[{"first_name":"Stephanie","last_name":"zur Nedden","id":"3C77F464-F248-11E8-B48F-1D18A9856A87","full_name":"zur Nedden, Stephanie"},{"first_name":"Alexander S.","last_name":"Doney","full_name":"Doney, Alexander S."},{"full_name":"Frenguelli, Bruno G.","last_name":"Frenguelli","first_name":"Bruno G."}],"publisher":"Springer","department":[{"_id":"HaJa"}],"editor":[{"full_name":"Masino, Susan","last_name":"Masino","first_name":"Susan"},{"last_name":"Boison","first_name":"Detlev","full_name":"Boison, Detlev"}],"title":"The double-edged sword: Gaining Adenosine at the expense of ATP. How to balance the books","status":"public","publication_status":"published","_id":"10896","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","year":"2012","acknowledgement":"We are grateful to Research into Ageing/Ageing UK and The Dunhill Trust for funding SzN’s graduate studies, and to Prof Nicholas Dale for his valuable input.","abstract":[{"text":"Under physiological conditions the brain, via the purine salvage pathway, reuses the preformed purine bases hypoxanthine, derived from ATP degradation, and adenine (Ade), derived from polyamine synthesis, to restore its ATP pool. However, the massive degradation of ATP during ischemia, although providing valuable neuroprotective adenosine, results in the accumulation and loss of diffusible purine metabolites and thereby leads to a protracted reduction in the post-ischemic ATP pool size. In vivo, this may both limit the ability to deploy ATP-dependent reparative mechanisms and reduce the subsequent availability of adenosine, whilst in brain slices results in tissue with substantially lower levels of ATP than in vivo. In the present review, we describe the mechanisms by which brain tissue replenishes its ATP, how this can be improved with the clinically tolerated chemicals D-ribose and adenine, and the functional, and potential therapeutic, implications of doing so.","lang":"eng"}],"place":"New York","type":"book_chapter","language":[{"iso":"eng"}],"doi":"10.1007/978-1-4614-3903-5_6","date_published":"2012-07-23T00:00:00Z","page":"109-129","quality_controlled":"1","citation":{"ieee":"S. zur Nedden, A. S. Doney, and B. G. Frenguelli, “The double-edged sword: Gaining Adenosine at the expense of ATP. How to balance the books,” in Adenosine, 1st ed., S. Masino and D. Boison, Eds. New York: Springer, 2012, pp. 109–129.","apa":"zur Nedden, S., Doney, A. S., & Frenguelli, B. G. (2012). The double-edged sword: Gaining Adenosine at the expense of ATP. How to balance the books. In S. Masino & D. Boison (Eds.), Adenosine (1st ed., pp. 109–129). New York: Springer. https://doi.org/10.1007/978-1-4614-3903-5_6","ista":"zur Nedden S, Doney AS, Frenguelli BG. 2012.The double-edged sword: Gaining Adenosine at the expense of ATP. How to balance the books. In: Adenosine. , 109–129.","ama":"zur Nedden S, Doney AS, Frenguelli BG. The double-edged sword: Gaining Adenosine at the expense of ATP. How to balance the books. In: Masino S, Boison D, eds. Adenosine. 1st ed. New York: Springer; 2012:109-129. doi:10.1007/978-1-4614-3903-5_6","chicago":"Nedden, Stephanie zur, Alexander S. Doney, and Bruno G. Frenguelli. “The Double-Edged Sword: Gaining Adenosine at the Expense of ATP. How to Balance the Books.” In Adenosine, edited by Susan Masino and Detlev Boison, 1st ed., 109–29. New York: Springer, 2012. https://doi.org/10.1007/978-1-4614-3903-5_6.","short":"S. zur Nedden, A.S. Doney, B.G. Frenguelli, in:, S. Masino, D. Boison (Eds.), Adenosine, 1st ed., Springer, New York, 2012, pp. 109–129.","mla":"zur Nedden, Stephanie, et al. “The Double-Edged Sword: Gaining Adenosine at the Expense of ATP. How to Balance the Books.” Adenosine, edited by Susan Masino and Detlev Boison, 1st ed., Springer, 2012, pp. 109–29, doi:10.1007/978-1-4614-3903-5_6."},"publication":"Adenosine","article_processing_charge":"No","publication_identifier":{"eisbn":["9781461439035"],"isbn":["9781461439028"]},"day":"23","month":"07","scopus_import":"1"},{"oa_version":"None","intvolume":" 24","title":"Outfits for different occasions: tissue-specific roles of Nuclear Envelope proteins","status":"public","_id":"11089","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","issue":"6","abstract":[{"lang":"eng","text":"The Nuclear Envelope (NE) contains over 100 different proteins that associate with nuclear components such as chromatin, the lamina and the transcription machinery. Mutations in genes encoding NE proteins have been shown to result in tissue-specific defects and disease, suggesting cell-type specific differences in NE composition and function. Consistent with these observations, recent studies have revealed unexpected functions for numerous NE associated proteins during cell differentiation and development. Here we review the latest insights into the roles played by the NE in cell differentiation, development, disease and aging, focusing primarily on inner nuclear membrane (INM) proteins and nuclear pore components."}],"type":"journal_article","date_published":"2012-12-01T00:00:00Z","page":"775-783","article_type":"original","citation":{"ama":"Gomez-Cavazos JS, Hetzer M. Outfits for different occasions: tissue-specific roles of Nuclear Envelope proteins. Current Opinion in Cell Biology. 2012;24(6):775-783. doi:10.1016/j.ceb.2012.08.008","ista":"Gomez-Cavazos JS, Hetzer M. 2012. Outfits for different occasions: tissue-specific roles of Nuclear Envelope proteins. Current Opinion in Cell Biology. 24(6), 775–783.","apa":"Gomez-Cavazos, J. S., & Hetzer, M. (2012). Outfits for different occasions: tissue-specific roles of Nuclear Envelope proteins. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2012.08.008","ieee":"J. S. Gomez-Cavazos and M. Hetzer, “Outfits for different occasions: tissue-specific roles of Nuclear Envelope proteins,” Current Opinion in Cell Biology, vol. 24, no. 6. Elsevier, pp. 775–783, 2012.","mla":"Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “Outfits for Different Occasions: Tissue-Specific Roles of Nuclear Envelope Proteins.” Current Opinion in Cell Biology, vol. 24, no. 6, Elsevier, 2012, pp. 775–83, doi:10.1016/j.ceb.2012.08.008.","short":"J.S. Gomez-Cavazos, M. Hetzer, Current Opinion in Cell Biology 24 (2012) 775–783.","chicago":"Gomez-Cavazos, J Sebastian, and Martin Hetzer. “Outfits for Different Occasions: Tissue-Specific Roles of Nuclear Envelope Proteins.” Current Opinion in Cell Biology. Elsevier, 2012. https://doi.org/10.1016/j.ceb.2012.08.008."},"publication":"Current Opinion in Cell Biology","article_processing_charge":"No","day":"01","keyword":["Cell Biology"],"scopus_import":"1","volume":24,"date_updated":"2022-07-18T08:38:47Z","date_created":"2022-04-07T07:51:37Z","author":[{"full_name":"Gomez-Cavazos, J Sebastian","first_name":"J Sebastian","last_name":"Gomez-Cavazos"},{"full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","last_name":"HETZER","first_name":"Martin W"}],"publisher":"Elsevier","publication_status":"published","pmid":1,"year":"2012","extern":"1","language":[{"iso":"eng"}],"doi":"10.1016/j.ceb.2012.08.008","quality_controlled":"1","external_id":{"pmid":["22995343"]},"publication_identifier":{"issn":["0955-0674"]},"month":"12"},{"keyword":["Cell Biology"],"scopus_import":"1","day":"01","article_processing_charge":"No","article_type":"original","page":"88-100","publication":"Nucleus","citation":{"ama":"Vargas JD, Hatch EM, Anderson DJ, Hetzer M. Transient nuclear envelope rupturing during interphase in human cancer cells. Nucleus. 2012;3(1):88-100. doi:10.4161/nucl.18954","ieee":"J. D. Vargas, E. M. Hatch, D. J. Anderson, and M. Hetzer, “Transient nuclear envelope rupturing during interphase in human cancer cells,” Nucleus, vol. 3, no. 1. Taylor & Francis, pp. 88–100, 2012.","apa":"Vargas, J. D., Hatch, E. M., Anderson, D. J., & Hetzer, M. (2012). Transient nuclear envelope rupturing during interphase in human cancer cells. Nucleus. Taylor & Francis. https://doi.org/10.4161/nucl.18954","ista":"Vargas JD, Hatch EM, Anderson DJ, Hetzer M. 2012. Transient nuclear envelope rupturing during interphase in human cancer cells. Nucleus. 3(1), 88–100.","short":"J.D. Vargas, E.M. Hatch, D.J. Anderson, M. Hetzer, Nucleus 3 (2012) 88–100.","mla":"Vargas, Jesse D., et al. “Transient Nuclear Envelope Rupturing during Interphase in Human Cancer Cells.” Nucleus, vol. 3, no. 1, Taylor & Francis, 2012, pp. 88–100, doi:10.4161/nucl.18954.","chicago":"Vargas, Jesse D., Emily M. Hatch, Daniel J. Anderson, and Martin Hetzer. “Transient Nuclear Envelope Rupturing during Interphase in Human Cancer Cells.” Nucleus. Taylor & Francis, 2012. https://doi.org/10.4161/nucl.18954."},"date_published":"2012-01-01T00:00:00Z","type":"journal_article","abstract":[{"text":"Neoplastic cells are often characterized by specific morphological abnormalities of the nuclear envelope (NE), which have been used for cancer diagnosis for more than a century. The NE is a double phospholipid bilayer that encapsulates the nuclear genome, regulates all nuclear trafficking of RNAs and proteins and prevents the passive diffusion of macromolecules between the nucleoplasm and the cytoplasm. Whether there is a consequence to the proper functioning of the cell and loss of structural integrity of the nucleus remains unclear. Using live cell imaging, we characterize a phenomenon wherein nuclei of several proliferating human cancer cell lines become temporarily ruptured during interphase. Strikingly, NE rupturing was associated with the mislocalization of nucleoplasmic and cytoplasmic proteins and, in the most extreme cases, the entrapment of cytoplasmic organelles in the nuclear interior. In addition, we observed the formation of micronuclei-like structures during interphase and the movement of chromatin out of the nuclear space. The frequency of these NE rupturing events was higher in cells in which the nuclear lamina, a network of intermediate filaments providing mechanical support to the NE, was not properly formed. Our data uncover the existence of a NE instability that has the potential to change the genomic landscape of cancer cells.","lang":"eng"}],"issue":"1","title":"Transient nuclear envelope rupturing during interphase in human cancer cells","status":"public","intvolume":" 3","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","_id":"11091","oa_version":"None","month":"01","publication_identifier":{"issn":["1949-1034"],"eissn":["1949-1042"]},"quality_controlled":"1","external_id":{"pmid":["22567193"]},"language":[{"iso":"eng"}],"doi":"10.4161/nucl.18954","extern":"1","publication_status":"published","publisher":"Taylor & Francis","year":"2012","pmid":1,"date_created":"2022-04-07T07:51:53Z","date_updated":"2022-07-18T08:52:53Z","volume":3,"author":[{"full_name":"Vargas, Jesse D.","last_name":"Vargas","first_name":"Jesse D."},{"last_name":"Hatch","first_name":"Emily M.","full_name":"Hatch, Emily M."},{"last_name":"Anderson","first_name":"Daniel J.","full_name":"Anderson, Daniel J."},{"full_name":"HETZER, Martin W","first_name":"Martin W","last_name":"HETZER","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X"}]},{"quality_controlled":"1","external_id":{"pmid":["22264802"]},"oa":1,"main_file_link":[{"url":"https://doi.org/10.1016/j.devcel.2011.11.021","open_access":"1"}],"language":[{"iso":"eng"}],"doi":"10.1016/j.devcel.2011.11.021","publication_identifier":{"issn":["1534-5807"]},"month":"01","publisher":"Elsevier","publication_status":"published","pmid":1,"year":"2012","volume":22,"date_updated":"2022-07-18T08:53:16Z","date_created":"2022-04-07T07:52:10Z","author":[{"first_name":"Maximiliano A.","last_name":"D'Angelo","full_name":"D'Angelo, Maximiliano A."},{"last_name":"Gomez-Cavazos","first_name":"J. Sebastian","full_name":"Gomez-Cavazos, J. Sebastian"},{"last_name":"Mei","first_name":"Arianna","full_name":"Mei, Arianna"},{"full_name":"Lackner, Daniel H.","first_name":"Daniel H.","last_name":"Lackner"},{"last_name":"HETZER","first_name":"Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","full_name":"HETZER, Martin W"}],"extern":"1","page":"446-458","article_type":"original","citation":{"mla":"D’Angelo, Maximiliano A., et al. “A Change in Nuclear Pore Complex Composition Regulates Cell Differentiation.” Developmental Cell, vol. 22, no. 2, Elsevier, 2012, pp. 446–58, doi:10.1016/j.devcel.2011.11.021.","short":"M.A. D’Angelo, J.S. Gomez-Cavazos, A. Mei, D.H. Lackner, M. Hetzer, Developmental Cell 22 (2012) 446–458.","chicago":"D’Angelo, Maximiliano A., J. Sebastian Gomez-Cavazos, Arianna Mei, Daniel H. Lackner, and Martin Hetzer. “A Change in Nuclear Pore Complex Composition Regulates Cell Differentiation.” Developmental Cell. Elsevier, 2012. https://doi.org/10.1016/j.devcel.2011.11.021.","ama":"D’Angelo MA, Gomez-Cavazos JS, Mei A, Lackner DH, Hetzer M. A change in nuclear pore complex composition regulates cell differentiation. Developmental Cell. 2012;22(2):446-458. doi:10.1016/j.devcel.2011.11.021","ista":"D’Angelo MA, Gomez-Cavazos JS, Mei A, Lackner DH, Hetzer M. 2012. A change in nuclear pore complex composition regulates cell differentiation. Developmental Cell. 22(2), 446–458.","apa":"D’Angelo, M. A., Gomez-Cavazos, J. S., Mei, A., Lackner, D. H., & Hetzer, M. (2012). A change in nuclear pore complex composition regulates cell differentiation. Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2011.11.021","ieee":"M. A. D’Angelo, J. S. Gomez-Cavazos, A. Mei, D. H. Lackner, and M. Hetzer, “A change in nuclear pore complex composition regulates cell differentiation,” Developmental Cell, vol. 22, no. 2. Elsevier, pp. 446–458, 2012."},"publication":"Developmental Cell","date_published":"2012-01-19T00:00:00Z","keyword":["Developmental Biology","Cell Biology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology"],"scopus_import":"1","article_processing_charge":"No","day":"19","intvolume":" 22","status":"public","title":"A change in nuclear pore complex composition regulates cell differentiation","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","_id":"11093","oa_version":"Published Version","type":"journal_article","issue":"2","abstract":[{"text":"Nuclear pore complexes (NPCs) are built from ∼30 different proteins called nucleoporins or Nups. Previous studies have shown that several Nups exhibit cell-type-specific expression and that mutations in NPC components result in tissue-specific diseases. Here we show that a specific change in NPC composition is required for both myogenic and neuronal differentiation. The transmembrane nucleoporin Nup210 is absent in proliferating myoblasts and embryonic stem cells (ESCs) but becomes expressed and incorporated into NPCs during cell differentiation. Preventing Nup210 production by RNAi blocks myogenesis and the differentiation of ESCs into neuroprogenitors. We found that the addition of Nup210 to NPCs does not affect nuclear transport but is required for the induction of genes that are essential for cell differentiation. Our results identify a single change in NPC composition as an essential step in cell differentiation and establish a role for Nup210 in gene expression regulation and cell fate determination.","lang":"eng"}]},{"oa_version":"None","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","_id":"11092","status":"public","title":"Extremely long-lived nuclear pore proteins in the rat brain","intvolume":" 335","abstract":[{"lang":"eng","text":"To combat the functional decline of the proteome, cells use the process of protein turnover to replace potentially impaired polypeptides with new functional copies. We found that extremely long-lived proteins (ELLPs) did not turn over in postmitotic cells of the rat central nervous system. These ELLPs were associated with chromatin and the nuclear pore complex, the central transport channels that mediate all molecular trafficking in and out of the nucleus. The longevity of these proteins would be expected to expose them to potentially harmful metabolites, putting them at risk of accumulating damage over extended periods of time. Thus, it is possible that failure to maintain proper levels and functional integrity of ELLPs in nonproliferative cells might contribute to age-related deterioration in cell and tissue function."}],"issue":"6071","type":"journal_article","date_published":"2012-02-02T00:00:00Z","publication":"Science","citation":{"mla":"Savas, Jeffrey N., et al. “Extremely Long-Lived Nuclear Pore Proteins in the Rat Brain.” Science, vol. 335, no. 6071, American Association for the Advancement of Science, 2012, pp. 942–942, doi:10.1126/science.1217421.","short":"J.N. Savas, B.H. Toyama, T. Xu, J.R. Yates, M. Hetzer, Science 335 (2012) 942–942.","chicago":"Savas, Jeffrey N., Brandon H. Toyama, Tao Xu, John R. Yates, and Martin Hetzer. “Extremely Long-Lived Nuclear Pore Proteins in the Rat Brain.” Science. American Association for the Advancement of Science, 2012. https://doi.org/10.1126/science.1217421.","ama":"Savas JN, Toyama BH, Xu T, Yates JR, Hetzer M. Extremely long-lived nuclear pore proteins in the rat brain. Science. 2012;335(6071):942-942. doi:10.1126/science.1217421","ista":"Savas JN, Toyama BH, Xu T, Yates JR, Hetzer M. 2012. Extremely long-lived nuclear pore proteins in the rat brain. Science. 335(6071), 942–942.","apa":"Savas, J. N., Toyama, B. H., Xu, T., Yates, J. R., & Hetzer, M. (2012). Extremely long-lived nuclear pore proteins in the rat brain. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1217421","ieee":"J. N. Savas, B. H. Toyama, T. Xu, J. R. Yates, and M. Hetzer, “Extremely long-lived nuclear pore proteins in the rat brain,” Science, vol. 335, no. 6071. American Association for the Advancement of Science, pp. 942–942, 2012."},"article_type":"letter_note","page":"942-942","day":"02","article_processing_charge":"No","scopus_import":"1","keyword":["Multidisciplinary"],"author":[{"last_name":"Savas","first_name":"Jeffrey N.","full_name":"Savas, Jeffrey N."},{"last_name":"Toyama","first_name":"Brandon H.","full_name":"Toyama, Brandon H."},{"last_name":"Xu","first_name":"Tao","full_name":"Xu, Tao"},{"last_name":"Yates","first_name":"John R.","full_name":"Yates, John R."},{"full_name":"HETZER, Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","first_name":"Martin W","last_name":"HETZER"}],"date_created":"2022-04-07T07:52:01Z","date_updated":"2022-07-18T08:53:06Z","volume":335,"year":"2012","pmid":1,"publication_status":"published","publisher":"American Association for the Advancement of Science","extern":"1","doi":"10.1126/science.1217421","language":[{"iso":"eng"}],"external_id":{"pmid":["22300851"]},"quality_controlled":"1","month":"02","publication_identifier":{"issn":["0036-8075"],"eissn":["1095-9203"]}}]