Sökning: onr:"swepub:oai:prod.swepub.kib.ki.se:143639759" > Methylation deficie...
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000 | 02864naa a2200553 4500 | |
001 | oai:prod.swepub.kib.ki.se:143639759 | |
003 | SwePub | |
008 | 240811s2020 | |||||||||||000 ||eng| | |
024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1436397592 URI |
024 | 7 | a https://doi.org/10.1038/s42003-020-0942-02 DOI |
040 | a (SwePub)ki | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Fustin, JM4 aut |
245 | 1 0 | a Methylation deficiency disrupts biological rhythms from bacteria to humans |
264 | c 2020-05-06 | |
264 | 1 | b Springer Science and Business Media LLC,c 2020 |
520 | a The methyl cycle is a universal metabolic pathway providing methyl groups for the methylation of nuclei acids and proteins, regulating all aspects of cellular physiology. We have previously shown that methyl cycle inhibition in mammals strongly affects circadian rhythms. Since the methyl cycle and circadian clocks have evolved early during evolution and operate in organisms across the tree of life, we sought to determine whether the link between the two is also conserved. Here, we show that methyl cycle inhibition affects biological rhythms in species ranging from unicellular algae to humans, separated by more than 1 billion years of evolution. In contrast, the cyanobacterial clock is resistant to methyl cycle inhibition, although we demonstrate that methylations themselves regulate circadian rhythms in this organism. Mammalian cells with a rewired bacteria-like methyl cycle are protected, like cyanobacteria, from methyl cycle inhibition, providing interesting new possibilities for the treatment of methylation deficiencies. | |
700 | 1 | a Ye, SQ4 aut |
700 | 1 | a Rakers, C4 aut |
700 | 1 | a Kaneko, K4 aut |
700 | 1 | a Fukumoto, K4 aut |
700 | 1 | a Yamano, M4 aut |
700 | 1 | a Versteven, M4 aut |
700 | 1 | a Grunewald, E4 aut |
700 | 1 | a Cargill, SJ4 aut |
700 | 1 | a Tamai, TK4 aut |
700 | 1 | a Xu, Y4 aut |
700 | 1 | a Jabbur, ML4 aut |
700 | 1 | a Kojima, R4 aut |
700 | 1 | a Lamberti, ML4 aut |
700 | 1 | a Yoshioka-Kobayashi, K4 aut |
700 | 1 | a Whitmore, D4 aut |
700 | 1 | a Tammam, S4 aut |
700 | 1 | a Howell, PL4 aut |
700 | 1 | a Kageyama, R4 aut |
700 | 1 | a Matsuo, T4 aut |
700 | 1 | a Stanewsky, R4 aut |
700 | 1 | a Golombek, DA4 aut |
700 | 1 | a Johnson, CH4 aut |
700 | 1 | a Kakeya, H4 aut |
700 | 1 | a van Ooijen, G4 aut |
700 | 1 | a Okamura, H4 aut |
773 | 0 | t Communications biologyd : Springer Science and Business Media LLCg 3:1, s. 211-q 3:1<211-x 2399-3642 |
856 | 4 | u https://www.nature.com/articles/s42003-020-0942-0.pdf |
856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:143639759 |
856 | 4 8 | u https://doi.org/10.1038/s42003-020-0942-0 |
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