Results 61 to 70 of about 14,089,637 (300)
From mice to humans—divergent strategies for intestinal homeostasis and regeneration
Recent advances such as organoid genome editing, xenotransplantation, imaging, and whole‐genome sequencing have enabled direct studies of human intestinal stem cells (ISCs). These studies reveal species‐specific features, including slower ISC proliferation, distinct injury responses, slower somatic mutation accumulation in humans, and an inverse ...
Keiko Ishikawa +2 more
wiley +1 more source
Reconstructing enzyme evolution by protein engineering
Natural enzyme evolution can be retraced by protein engineering methods such as directed evolution, rational design, and ancestral sequence reconstruction. These approaches reveal how enzymes emerged from ligand‐binding scaffolds, developed varying substrate preferences, formed oligomeric complexes, adapted to environmental changes, and evolved novel ...
Lukas Drexler +2 more
wiley +1 more source
Peripheral lysosomes recruit PLEKHG3 to focal adhesions and restrain protrusion dynamics
Proximity‐dependent labeling at the LAMTOR complex revealed the Rho GEF PLEKHG3 as a lysosome‐proximal protein directing the study toward the influence of lysosome positioning on actin dynamics and cell motility. We show that PLEKHG3 colocalizes with lysosomes at focal adhesion sites and observe that forced peripheral dispersion of lysosomes hinders ...
Rainer Ettelt +8 more
wiley +1 more source
Liver organoids: modelling complexity in homeostasis and disease
Studying liver in vitro has been challenging because simple 2D cell cultures fail to capture liver's cellular and architectural complexity. To bridge this gap, scientists increasingly use organoids, 3D liver models which better mimic liver composition and function. This review examines recent advances in liver organoid complexity and realism, discusses
Anna M. Dowbaj, Meritxell Huch
wiley +1 more source
This review focuses on the role of autophagy and mitophagy in maintaining pancreatic β‐cell function and homeostasis. We discuss how genetic defects affecting these pathways contribute to the development of type 1, type 2, monogenic, and gestational diabetes. We further explore their potential as therapeutic targets. Created in BioRender.
Yunkyeong Lee +2 more
wiley +1 more source
Obesity raises blood levels of PAI‐1, a protein linked to metabolic dysfunction‐associated steatotic liver disease in people with obesity. In female mice fed a high‐fat diet, partially lowering PAI‐1 led to smaller subcutaneous fat cells and lower liver cholesterol, without changing body weight or insulin sensitivity.
Claudia E. Ramirez Bustamante +10 more
wiley +1 more source
Emerging experimental and computational methods for studying redox‐regulated structural transitions
Redox reactions can reshape proteins and alter how they behave in cells, with important consequences for health and disease. This review explores emerging experimental and computational approaches for discovering these redox‐sensitive protein switches, revealing their structural effects, and predicting their behavior, opening new opportunities to ...
Tasneem Rass +2 more
wiley +1 more source
Synergistic perspectives—How single‐molecule biophysics complement biochemical understanding
In this review, we discuss how ensemble biochemistry and single‐molecule approaches are complementary, outline commonly used single‐molecule techniques, and illustrate their relevance through two representative case studies: chromatin organization by SMC complexes and pathway choice during DNA double‐strand break repair.
Sara De Bragança +2 more
wiley +1 more source
Mycobacterial 3‐methylcrotonyl‐CoA carboxylase uses a mobile biotin‐carrying domain to shuttle a carboxyl group between two catalytic sites, enabling carboxylation of 3‐methylcrotonyl‐CoA during leucine breakdown. Cryo‐electron microscopy captures the carrier at both sites and reveals an inward loop movement that may prevent futile rebinding to the ...
Ajit Yadav +2 more
wiley +1 more source
How do genomes gain new functional parts? In eukaryotes, which tend to evolve under weak selection, much of the genome is junk. Palazzo and Qiu borrow the logic of Markov chains to show how non‐functional DNA becomes functional through the appearance of intermediate states, which arise due to epistasis, buffering, and biochemical messiness, allowing ...
Alexander F. Palazzo, Yi Qiu
wiley +1 more source

