{"publisher":"American Association for the Advancement of Science","article_type":"letter_note","year":"2012","day":"02","date_published":"2012-02-02T00:00:00Z","pmid":1,"keyword":["Multidisciplinary"],"scopus_import":"1","quality_controlled":"1","title":"Extremely long-lived nuclear pore proteins in the rat brain","issue":"6071","oa_version":"None","intvolume":" 335","language":[{"iso":"eng"}],"status":"public","page":"942-942","external_id":{"pmid":["22300851"]},"user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","article_processing_charge":"No","citation":{"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.","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","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","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.","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."},"month":"02","date_created":"2022-04-07T07:52:01Z","_id":"11092","doi":"10.1126/science.1217421","author":[{"first_name":"Jeffrey N.","full_name":"Savas, Jeffrey N.","last_name":"Savas"},{"first_name":"Brandon H.","full_name":"Toyama, Brandon H.","last_name":"Toyama"},{"last_name":"Xu","full_name":"Xu, Tao","first_name":"Tao"},{"full_name":"Yates, John R.","first_name":"John R.","last_name":"Yates"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","last_name":"HETZER","orcid":"0000-0002-2111-992X","first_name":"Martin W","full_name":"HETZER, Martin W"}],"publication":"Science","publication_status":"published","abstract":[{"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.","lang":"eng"}],"date_updated":"2022-07-18T08:53:06Z","volume":335,"extern":"1","type":"journal_article","publication_identifier":{"issn":["0036-8075"],"eissn":["1095-9203"]}}