Liyan Jia, Yan Qiao · 2025 · Journal of the American Chemical Society · ACS Publications · added 2026-04-20
In nature, life is inherently dissipative. Cells continuously consume energy (such as ATP) to sustain homeostasis, drive metabolism, and respond dynamically to environmental cues. Inspired by this pri Show more
In nature, life is inherently dissipative. Cells continuously consume energy (such as ATP) to sustain homeostasis, drive metabolism, and respond dynamically to environmental cues. Inspired by this principle, we develop a synthetic protocell system that exhibits dissipative behavior and initiates metabolic-like processes. Our design features synthetic vesicles formed from a cationic surfactant, which undergo a fuel-driven transformation into coacervate protocells via liquid-liquid phase separation. Dissipation is achieved through alkaline phosphatase (ALP)-catalyzed ATP hydrolysis, driving the reverse transition from coacervates back to vesicles. The distinct physicochemical properties and internal organization of vesicle and coacervate protocells enable us to design functional regulators capable of producing secondary signals, such as fluorescence and enzymatic products. This work offers a strategy for engineering enzymatic reaction-regulated dissipative behaviors of protocell systems that emulate key aspects of cellular metabolism, representing a step toward synthetic life-like systems with dynamic behavior and functional complexity. Show less
Despite the vast number of enzymatic kinetic measurements reported across decades of biochemical literature, the majority of relational enzyme kinetic data—linking amino acid sequence, substrate ident Show more
Despite the vast number of enzymatic kinetic measurements reported across decades of biochemical literature, the majority of relational enzyme kinetic data—linking amino acid sequence, substrate identity, kinetic parameters, and assay conditions—remains uncollected and inaccessible in structured form. This constitutes a significant portion of the “dark matter” of enzymology. Unlocking these hidden data through automated extraction offers an opportunity to expand enzyme dataset diversity and size, critical Show less
2024 · Scientific Data · Nature · added 2026-04-21
11,571 — — NER 2008 SCAI33 1,206 — — NER 2012 ADE39 300 case reports 5,063 drugs — 6,821 drug adverse effects 279 drug dosage RE 2013 DDI43 1,025, including texts from DrugBank and 18,502 drugs — 5,02 Show more
11,571 — — NER 2008 SCAI33 1,206 — — NER 2012 ADE39 300 case reports 5,063 drugs — 6,821 drug adverse effects 279 drug dosage RE 2013 DDI43 1,025, including texts from DrugBank and 18,502 drugs — 5,028 drug-drug interactions RE 2015 CHEMDNER34 84,355 chemicals — — NER 2016 BC5CDR 1,500 articles 15,935 chemicals 12,850 diseases 4,409 MeSH chemically induced diseases NER, NEN, RE 2017 N-ary drug-gene-mutation 35 — — — 137,469 drug–gene 3,192 drug–mutation RE 2017 40 ChemProt 32,514 chemicals 30,922 genes Show less
2018 · Oxidative Medicine and Cellular Longevity · added 2026-04-21
Metabolic reprogramming is one of the hallmarks of cancer. Nrf2 pathway is one of the critical signaling cascades involved in cell defense and survival against oxidative stress. The significance of Nr Show more
Metabolic reprogramming is one of the hallmarks of cancer. Nrf2 pathway is one of the critical signaling cascades involved in cell defense and survival against oxidative stress. The significance of Nrf2 in cancer metabolism begins to be recognized. In this minireview, we focus on the Nrf2-mediated cancer metabolic reprogramming and intend to highlight the role of Nrf2 in the regulation of malignant transformation, cancer proliferation, and the development of treatment resistance via metabolic adaptations. We hope for the development of noninvasive biomarkers and novel therapeutic approaches for cancer based on Nrf2-directed cancer metabolic reprogramming in the near future. Show less