Proteomics research has developed until recently in a relative isolation from other fast-moving disciplines such as ecology and evolution. This is unfortunate since applying proteomics to these disciplines has apparently the potential to open new perspectives. The huge majority of species indeed exhibit over their entire geographic range a metapopulation structure, occupying habitats that are fragmented and heterogeneous in space and/or through time. Traditionally, population genetics is the main tool used to studying metatopulations, as it describes the spatial structure of populations and the level of gene flow between them. In this Viewpoint, we present the reasons why we think that proteomics, because of the level of integration it promotes, has the potential to resolve interesting issues specific to metapopulation biology and adaptive processes.
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http://dx.doi.org/10.1002/pmic.200500423 | DOI Listing |
Free Radic Biol Med
January 2025
Laboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, South Korea. Electronic address:
Human embryonic stem cells (hESCs) and their extracellular vesicles (EVs) hold significant potential for tissue repair and regeneration. Neural stem cells (NSCs) in the adult brain often acquire senescent phenotypes after ischemic injuries, releasing neurodegenerative senescence-associated secretory phenotype factors. In this study, we investigated the senotherapeutic effects of hESC-EVs on NSCs and confirmed their neuroprotective effects in neurons via rejuvenation of NSC secretions.
View Article and Find Full Text PDFAugmented extracellular matrix (ECM) stiffness is a mechanical hallmark of cancer. Mechanotransduction studies have extensively probed the mechanisms by which ECM stiffness regulates intracellular communication. However, the influence of stiffness on intercellular communication aiding tumor progression in three-dimensional microenvironments remains unknown.
View Article and Find Full Text PDFAutoimmunity affects 10% of the population. Within this umbrella, autoantibody-mediated diseases targeting one autoantigen provide a unique opportunity to comprehensively understand the developmental pathway of disease-causing B cells and autoantibodies. While such autoreactivities are believed to be generated during germinal centre reactions, the roles of earlier immune checkpoints in autoantigen-specific B cell tolerance are poorly understood.
View Article and Find Full Text PDFThe expression of genomically-encoded information is not error-free. Transcript-error rates are dramatically higher than DNA-level mutation rates, and despite their transient nature, the steady-state load of such errors must impose some burden on cellular performance. However, a broad perspective on the degree to which transcript-error rates are constrained by natural selection and diverge among lineages remains to be developed.
View Article and Find Full Text PDFBrain
January 2025
Medical Research Council Prion Unit, University College London Institute of Prion Diseases, London, W1W 7FF, UK.
Prions are assemblies of misfolded prion protein that cause several fatal and transmissible neurodegenerative diseases, with the most common phenotype in humans being sporadic Creutzfeldt-Jakob disease (sCJD). Aside from variation of the prion protein itself, molecular risk factors are not well understood. Prion and prion-like mechanisms are thought to underpin common neurodegenerative disorders meaning that the elucidation of mechanisms could have broad relevance.
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