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| Home > Publications Database > Dataset: RNA Selectively Modulates Activity of Virulent Amyloid PSMα3 and Host Defense LL-37 via Phase Separation and Aggregation Dynamics, v1 > print |
| 001 | 282946 | ||
| 005 | 20251218103447.0 | ||
| 024 | 7 | _ | |a 10.5281/ZENODO.17113344 |2 doi |
| 024 | 7 | _ | |a 10.5281/zenodo.17113344 |2 doi |
| 037 | _ | _ | |a DZNE-2025-01407 |
| 100 | 1 | _ | |a Rayan, Bader |0 0000-0003-1408-2214 |b 0 |
| 245 | _ | _ | |a Dataset: RNA Selectively Modulates Activity of Virulent Amyloid PSMα3 and Host Defense LL-37 via Phase Separation and Aggregation Dynamics, v1 |
| 260 | _ | _ | |c 2025 |b Zenodo |
| 336 | 7 | _ | |a MISC |2 BibTeX |
| 336 | 7 | _ | |a Dataset |b dataset |m dataset |0 PUB:(DE-HGF)32 |s 1765985962_5349 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a Chart or Table |0 26 |2 EndNote |
| 336 | 7 | _ | |a Dataset |2 DataCite |
| 336 | 7 | _ | |a DATA_SET |2 ORCID |
| 336 | 7 | _ | |a ResearchData |2 DINI |
| 520 | _ | _ | |a Amyloids, classically linked to neurodegenerative diseases, also play critical roles in infection and immunity. Phenol-soluble modulins (PSMs) from Staphylococcus aureus are virulent amyloids that contribute to cytotoxicity, immune modulation, and biofilm stability. PSMα3 forms cross-α amyloid fibrils and shares sequence and structural features with LL-37, a human host-defense peptide that assembles into α-helical structures. Here, we uncover RNA as a potent, context-dependent modulator of their aggregation and activity. RNA consistently reduces LL-37’s cytotoxicity toward human cells without compromising its antibacterial function, suggesting a selective host-protective mechanism. In contrast, RNA preserves PSMα3’s cytotoxic and antimicrobial activity over time, likely by promoting liquid–liquid phase separation (LLPS) and stabilizing bioactive fibrillar polymorphs, enabling S. aureus to fine-tune its virulence strategies. At higher concentrations, RNA drives both peptides toward distinct aggregated states, amorphous for LL-37 and fibrillar for PSMα3, underlying their divergent functional outcomes. The amyloid inhibitor EGCG abolishes the bioactivity of both PSMα3 and LL-37, overriding RNA’s modulatory effects. Together, our findings establish RNA as a key modulator of both virulent amyloids and host-defense peptides, with broad implications for microbial immune evasion, innate immunity, and amyloid-associated diseases. Moreover, they highlight phase transitions as a tunable mechanism for regulating peptide bioactivity and a promising therapeutic target across infectious and neurodegenerative conditions. |
| 536 | _ | _ | |a 352 - Disease Mechanisms (POF4-352) |0 G:(DE-HGF)POF4-352 |c POF4-352 |f POF IV |x 0 |
| 588 | _ | _ | |a Dataset connected to DataCite |
| 700 | 1 | _ | |a Barnea, Eilon |b 1 |
| 700 | 1 | _ | |a Indig, Rinat |b 2 |
| 700 | 1 | _ | |a Pantoja, Christian Felipe |0 P:(DE-2719)2812808 |b 3 |
| 700 | 1 | _ | |a Gayk, Jesse |b 4 |
| 700 | 1 | _ | |a Lupu-Haber, Yael |0 0000-0002-2601-4123 |b 5 |
| 700 | 1 | _ | |a Upcher, Alexander |0 0000-0002-0910-6552 |b 6 |
| 700 | 1 | _ | |a Argoetti, Amir |0 0000-0002-0412-003X |b 7 |
| 700 | 1 | _ | |a Larsen, Jacob |0 0000-0002-6782-0594 |b 8 |
| 700 | 1 | _ | |a Buell, Alexander |0 0000-0003-1161-3622 |b 9 |
| 700 | 1 | _ | |a Zweckstetter, Markus |0 P:(DE-2719)2810591 |b 10 |
| 700 | 1 | _ | |a Landau, Meytal |0 0000-0002-1743-3430 |b 11 |
| 773 | _ | _ | |a 10.5281/zenodo.17113344 |
| 787 | 0 | _ | |a Rayan, Bader et.al. |d Zenodo, 2025 |i RelatedTo |0 DZNE-2025-01406 |r |t Dataset: RNA Selectively Modulates Activity of Virulent Amyloid PSMα3 and Host Defense LL-37 via Phase Separation and Aggregation Dynamics, v2 |
| 909 | C | O | |o oai:pub.dzne.de:282946 |p VDB |
| 910 | 1 | _ | |a Deutsches Zentrum für Neurodegenerative Erkrankungen |0 I:(DE-588)1065079516 |k DZNE |b 3 |6 P:(DE-2719)2812808 |
| 910 | 1 | _ | |a Deutsches Zentrum für Neurodegenerative Erkrankungen |0 I:(DE-588)1065079516 |k DZNE |b 10 |6 P:(DE-2719)2810591 |
| 913 | 1 | _ | |a DE-HGF |b Gesundheit |l Neurodegenerative Diseases |1 G:(DE-HGF)POF4-350 |0 G:(DE-HGF)POF4-352 |3 G:(DE-HGF)POF4 |2 G:(DE-HGF)POF4-300 |4 G:(DE-HGF)POF |v Disease Mechanisms |x 0 |
| 914 | 1 | _ | |y 2025 |
| 920 | 1 | _ | |0 I:(DE-2719)1410001 |k AG Zweckstetter |l Translational Structural Biology |x 0 |
| 980 | _ | _ | |a dataset |
| 980 | _ | _ | |a VDB |
| 980 | _ | _ | |a I:(DE-2719)1410001 |
| 980 | _ | _ | |a UNRESTRICTED |
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