Results 31 to 40 of about 124 (124)
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
Conserved binding mode but diverse interfaces of MreC‐PBP2 interactions
The crystal structure of abMreC reveals a conserved two β‐barrel architecture and provides structural insights into its role within the bacterial elongasome. The abMreC–abPBP2 complex model identifies the molecular basis of MreC‐mediated PBP2 recognition, contributing to the regulation of peptidoglycan synthesis.
Hyunseok Jang +4 more
wiley +1 more source
An epithelial GPR35 isoform supports tumor‐associated transcriptional and metabolic phenotypes
GPR35 generates two functionally distinct isoforms with previously unresolved roles. GPR35‐short mediates immune‐cell chemotaxis, while GPR35‐long is enriched in colorectal cancer epithelium, where it supports increased metabolism, proliferation, and tumor‐associated transcriptional programs.
Jørgen D. Rønneberg +14 more
wiley +1 more source
Structure‐forward targeting of claudins with synthetic binders
Claudins form the paracellular barriers between epithelial and endothelial tissues at tight junctions and are targets for molecular binders with the goal of modulating barrier permeability. Claudin‐binding molecules are relevant in drug delivery or in altering claudin interactions with disease‐causing proteins.
Alex J. Vecchio
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
Engineering peptides into antibodies—opportunities and strategies for therapeutic innovation
Peptides and antibodies occupy complementary therapeutic niches. Peptides recognize difficult targets in a compact format, while antibodies add specificity, long half‐life, and effector functions. This review examines strategies that merge both modalities—peptide grafting into loops, terminal and Fc fusions, and bioconjugation—highlighting how ...
Jinling Wang +2 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
Epigenetic reprogramming of lineage switching in cancer
Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı +4 more
wiley +1 more source
The microbiome in human skin aging
Age‐related skin changes encompass the well‐known visible phenotypic alterations, together with microbiome dysbiosis and a series of molecular aging hallmarks. These hallmarks characterize not only a fully stablished aged phenotype but also the skin aging process itself.
Manuel Huerta Arana +3 more
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

