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Proteins are the key molecular players of life, carrying out their functions through interactions. Microfluidic technologies have emerged as powerful tools for studying protein interactions with exquisite sensitivity, resolution, and throughput. In this review, we highlight recent advances in microfluidic approaches for protein interaction studies. We first explore continuous-flow microfluidics, which utilize diffusion-based techniques and electrophoretic methods, before examining the role of droplet microfluidics in probing protein interactions. We provide an overview of the diverse applications of these technologies in biophysical research, drug discovery, and clinical diagnostics. We conclude with a discussion of the potential of microfluidics for driving future innovations and emerging opportunities.
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http://dx.doi.org/10.1007/s00249-025-01763-x | DOI Listing |
Genome Biol
September 2025
Department of Evolutionary Genetics, Max-Planck Institute for Evolutionary Biology, Plön, Germany.
Background: Most RNA-seq datasets harbor genes with extreme expression levels in some samples. Such extreme outliers are usually treated as technical errors and are removed from the data before further statistical analysis. Here we focus on the patterns of such outlier gene expression to investigate whether they provide insights into the underlying biology.
View Article and Find Full Text PDFEMBO J
September 2025
Department of Biology, University of Crete, Vassilika Vouton, Heraklion, 70013, Greece.
In the presence of chromatin bridges in cytokinesis, human cells retain actin-rich structures (actin patches) at the base of the intercellular canal to prevent chromosome breakage. Here, we show that daughter nuclei connected by chromatin bridges are under mechanical tension that requires interaction of the nuclear membrane Sun1/2-Nesprin-2 Linker of Nucleoskeleton and Cytoskeleton (LINC) complex with the actin cytoskeleton, and an intact nuclear lamina. This nuclear tension promotes accumulation of Sun1/2-Nesprin-2 proteins at the base of chromatin bridges and local enrichment of the RhoA-activator PDZ RhoGEF through PDZ-binding to cytoplasmic Nesprin-2 spectrin repeats.
View Article and Find Full Text PDFEMBO J
September 2025
New York University Grossman School of Medicine, Microbiology Department, New York, NY, USA.
Serine protease inhibitors (SERPINs) are involved in various physiological processes and diseases, such as inflammation, cancer metastasis, and neurodegeneration. Their role in viral infections is poorly understood, as their expression patterns during infection and the range of proteases they target have yet to be fully characterized. Here, we show widespread expression of human SERPINs in response to respiratory virus infections, both in bronchioalveolar lavages from COVID-19 patients and in polarized human airway epithelial cultures.
View Article and Find Full Text PDFCancer Metastasis Rev
September 2025
Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS, Gif-Sur-Yvette, 91198, France.
Integrins constitute a large and diverse family of cell adhesion molecules that play essential roles in regulating tumor cell differentiation, migration, proliferation, and neovascularization. Tumor cell-derived exosomes, a subtype of extracellular vesicles, are enriched with integrins that reflect their cells of origin. These exosomal integrins can promote extracellular matrix remodeling, immune suppression, and vascular remodeling and are closely linked to tumor progression and metastasis, acting as pivotal players in mediating organ-specific metastasis.
View Article and Find Full Text PDFNat Struct Mol Biol
September 2025
Developmental Epigenetics, Department of Biochemistry, University of Oxford, Oxford, UK.
X-chromosome inactivation (XCI) in mammals is orchestrated by the noncoding RNA X-inactive-specific transcript (Xist) that, together with specific interacting proteins, functions in cis to silence an entire X chromosome. Defined sites on Xist RNA carry the N-methyladenosine (mA) modification and perturbation of the mA writer complex has been found to abrogate Xist-mediated gene silencing. However, the relative contribution of mA and its mechanism of action remain unclear.
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