@article {70431,
	title = {De novo design of RNA pseudoknots with deep learning},
	journal = {bioRxiv},
	year = {2026},
	month = {2026 May 22},
	abstract = {<p>RNA design has been hindered by the limited accuracy of 3D structure prediction. Here, we show that intricate RNA structures can be generated with current deep learning tools through accurate de novo design of pseudoknot secondary structures. In an Eterna competition involving 57 pseudoknots, generative AI methods matched experienced human designers in solving most blind challenges, evaluated by single-nucleotide-resolution chemical mapping, compensatory mutagenesis, and cryogenic electron microscopy. Unexpectedly, AI-generated molecules with accurate secondary structures formed well-ordered 3D folds stabilized by noncanonical tertiary interactions not modeled during design. Success was guided by a RNet foundation model trained on prior chemical mapping data, suggesting that some difficult RNA design tasks may be tractable without first solving RNA 3D structure prediction.</p>
},
	doi = {10.64898/2026.05.21.726960},
	url = {https://www.biorxiv.org/content/early/2026/05/22/2026.05.21.726960},
	author = {Townley, Jill and Kladwang, Wipapat and Baker, David and Blair, Hamish M. and Choe, Christian A. and El Nesr, Gina and Favor, Andrew and Fisker, Eli and Haack, Daniel B. and He, Shujun and Hingey, Jason and Huang, Po-Ssu and Huang, Rui and Joshi, Chaitanya K. and Karagianes, Thomas and Kubaney, Andrew and Li{\`o}, Pietro and Mancino, Adamo and Romano, Jonathan and Rudolfs, Boris and Spellmon, Nicholas and Toor, Navtej and Wu, Vivian and Yu, Zhiheng and Eterna Participants and Das, Rhiju}
}
@article {47620,
	title = {Deacetylation of nuclear LC3 drives autophagy initiation under starvation.},
	journal = {Molecular cell},
	volume = {57},
	year = {2015},
	month = {2015 Feb 5},
	pages = {456-66},
	abstract = {<p>Shuttling of macromolecules between different cellular compartments helps regulate the timing and extent of different cellular activities. Here, we report that LC3, a key initiator of autophagy that cycles between the nucleus and cytoplasm, becomes selectively activated in the nucleus during starvation through deacetylation by the nuclear deacetylase Sirt1. Deacetylation of LC3 at K49 and K51 by Sirt1 allows LC3 to interact with the nuclear protein DOR and return to the cytoplasm with DOR, where it is able to bind Atg7 and other autophagy factors and undergo phosphatidylethanolamine conjugation to preautophagic membranes. The association of deacetylated LC3 with autophagic factors shifts LC3{\textquoteright}s distribution from the nucleus toward the cytoplasm. Thus, an acetylation-deacetylation cycle ensures that LC3 effectively redistributes in an activated form from nucleus to cytoplasm, where it plays a central role in autophagy to enable the cell to cope with the lack of external nutrients.</p>
},
	keywords = {Acetylation, Autophagy, Cell Nucleus, Cytoplasm, HEK293 Cells, Hela Cells, Humans, Lysine, Microscopy, Confocal, Microtubule-Associated Proteins, Sirtuin 1, Ubiquitin-Activating Enzymes},
	issn = {1097-4164},
	doi = {10.1016/j.molcel.2014.12.013},
	author = {Huang, Rui and Xu, Yinfeng and Wan, Wei and Shou, Xin and Qian, Jiali and You, Zhiyuan and Liu, Bo and Chang, Chunmei and Zhou, Tianhua and Lippincott-Schwartz, Jennifer and Liu, Wei}
}
