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Urolithin A Modulates PER2 Degradation via SIRT1 and Enhances the Amplitude of Circadian Clocks in Human Senescent Cells.
Nutrients
December 2024
Department of Neurobiology & Behavior, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.
Background/objectives: Circadian clocks are endogenous systems that regulate numerous biological, physiological, and behavioral events in living organisms. Aging attenuates the precision and robustness of circadian clocks, leading to prolonged and dampened circadian gene oscillation rhythms and amplitudes. This study investigated the effects of food-derived polyphenols such as ellagic acid and its metabolites (urolithin A, B, and C) on the aging clock at the cellular level using senescent human fibroblast cells, TIG-3 cells.
View Article and Find Full Text PDFTowards a Quantitative Description of Proteolysis: Contribution of Demasking and Hydrolysis Steps to Proteolysis Kinetics of Milk Proteins.
Foods
January 2025
A.N. Nesmeyanov Institute of Organoelement Compounds, Russian Academy of Sciences, 28 ul. Vavilova, Moscow 119991, Russia.
The hydrolysis of proteins by proteases (proteolysis) plays a significant role in biology and food science. Despite the importance of proteolysis, a universal quantitative model of this phenomenon has not yet been created. This review considers approaches to modeling proteolysis in a batch reactor that take into account differences in the hydrolysis of the individual peptide bonds, as well as the limited accessibility (masking) for the enzymes of some hydrolysis sites in the protein substrate.
View Article and Find Full Text PDFN-Degron PROTACs as a Potential Therapeutic Approach for Chronic Myeloid Leukemia.
Anticancer Agents Med Chem
January 2025
Department of Chemistry, Illinois State University, Normal, Il, USA.
Many oncoproteins are important therapeutic targets because of their critical role in inducing rapid cell proliferation, which represents one of the salient hallmarks of cancer. Chronic Myeloid Leukemia (CML) is a cancer of hematopoietic stem cells that is caused by the oncogene BCR-ABL1. BCR-ABL1 encodes a constitutively active tyrosine kinase protein that leads to the uncontrolled proliferation of myeloid cells, which is a hallmark of CML.
View Article and Find Full Text PDFET-PROTACs: modeling ternary complex interactions using cross-modal learning and ternary attention for accurate PROTAC-induced degradation prediction.
Brief Bioinform
November 2024
Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, Hunan 410003, China.
Motivation: Accurately predicting the degradation capabilities of proteolysis-targeting chimeras (PROTACs) for given target proteins and E3 ligases is important for PROTAC design. The distinctive ternary structure of PROTACs presents a challenge to traditional drug-target interaction prediction methods, necessitating more innovative approaches. While current state-of-the-art (SOTA) methods using graph neural networks (GNNs) can discern the molecular structure of PROTACs and proteins, thus enabling the efficient prediction of PROTACs' degradation capabilities, they rely heavily on limited crystal structure data of the POI-PROTAC-E3 ternary complex.
View Article and Find Full Text PDFDeciphering Polymer Interactions in Bioconjugates with Different Architectures by Structural Analysis via Time-resolved Limited Proteolysis Mass Spectrometry.
Angew Chem Int Ed Engl
January 2025
Julius-Maximilians-Universitat Wurzburg, Institute for Pharmacy and Chemistry, Am Hubland, 97074, Würzbrug, GERMANY.
Therapeutic proteins are commonly conjugated with polymers to modulate their pharmacokinetics but often lack a description of the polymer-protein interaction. We deployed limited proteolysis mass spectrometry (LiP-MS) to reveal the interaction of polyethylene glycol (PEG) and PEG alternative polymers with interferon-α2a (IFN). Target conjugates were digested with the specific protease trypsin and a "heavy" 15N-IFN wild type (IFN-WT) for time-resolved quantification of the cleavage dynamics.
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