Please use this identifier to cite or link to this item: https://doi.org/10.1038/s42003-021-02247-2
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dc.titleATP biphasically modulates LLPS of TDP-43 PLD by specifically binding arginine residues
dc.contributor.authorDang, Mei
dc.contributor.authorLim, Liangzhong
dc.contributor.authorKang, Jian
dc.contributor.authorSong, Jianxing
dc.date.accessioned2022-10-13T06:45:07Z
dc.date.available2022-10-13T06:45:07Z
dc.date.issued2021-06-10
dc.identifier.citationDang, Mei, Lim, Liangzhong, Kang, Jian, Song, Jianxing (2021-06-10). ATP biphasically modulates LLPS of TDP-43 PLD by specifically binding arginine residues. Communications Biology 4 (1) : 714. ScholarBank@NUS Repository. https://doi.org/10.1038/s42003-021-02247-2
dc.identifier.issn2399-3642
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/233050
dc.description.abstractMysteriously neurons maintain ATP concentrations of ~3 mM but whether ATP modulates TDP-43 LLPS remains completely unexplored. Here we characterized the effect of ATP on LLPS of TDP-43 PLD and seven mutants by DIC and NMR. The results revealed: 1) ATP induces and subsequently dissolves LLPS of TDP-43 PLD by specifically binding Arg saturated at 1:100. 2) ATP modifies the conformation-specific electrostatic property beyond just imposing screening effect. 3) Reversibility of LLPS of TDP-43 PLD and further exaggeration into aggregation appear to be controlled by a delicate network composed of both attractive and inhibitory interactions. Results together establish that ATP might be a universal but specific regulator for most, if not all, R-containing intrinsically-disordered regions by altering physicochemical properties, conformations, dynamics, LLPS and aggregation. Under physiological conditions, TDP-43 is highly bound with ATP and thus inhibited for LLPS, highlighting a central role of ATP in cell physiology, pathology and aging. © 2021, The Author(s).
dc.publisherNature Research
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceScopus OA2021
dc.typeArticle
dc.contributor.departmentDEPT OF BIOLOGICAL SCIENCES
dc.description.doi10.1038/s42003-021-02247-2
dc.description.sourcetitleCommunications Biology
dc.description.volume4
dc.description.issue1
dc.description.page714
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