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| http://dx.doi.org/10.3389/fimmu.2018.02110 | DOI Listing |
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Commentary on: Li et al.; Ca transients on the T cell surface trigger rapid integrin activation in a timescale of seconds. Nature Communications (2024).
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Department of Pharmacology, University of Virgnia School of Medicine, Charlottesville, VA 22908, United States.
Integrin αvβ3 Upregulation in Response to Nutrient Stress Promotes Lung Cancer Cell Metabolic Plasticity.
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Department of Pathology, Moores Cancer Center, and Sanford Consortium for Regenerative Medicine at the University of California, San Diego, La Jolla, California.
Unlabelled: Cancer stem/tumor-initiating cells display stress tolerance and metabolic flexibility to survive in a harsh environment with limited nutrient and oxygen availability. The molecular mechanisms underlying this phenomenon could provide targets to prevent metabolic adaptation and halt cancer progression. Here, we showed in cultured cells and live human surgical biopsies of non-small cell lung cancer that nutrient stress drives the expression of the epithelial cancer stem cell marker integrin αvβ3 via upregulation of the β3 subunit, resulting in a metabolic reprogramming cascade that allows tumor cells to thrive despite a nutrient-limiting environment.
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Osteoarthritis Cartilage
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Research Unit of Health Sciences and Technology, Faculty of Medicine, University of Oulu, Oulu, Finland; Department of Regenerative Medicine, State Research Institute Centre for Innovative Medicine, Vilnius, Lithuania; Department of Joint Surgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China; World Health Organization Collaborating Center for Public Health Aspects of Musculoskeletal Health and Aging, Université de Liège, Liège, Belgium.
Research conducted using murine preclinical models of osteoarthritis (OA) over the last three decades has brought forth many exciting developments showcasing mechanisms and pathways that drive disease pathogenesis. These models have identified therapeutic targets that can be modulated via innovative biologicals and pharmaceuticals. However, many of these approaches have failed to translate to humans and reach the clinic.
View Article and Find Full Text PDFCC16 drives VLA-2-dependent SPLUNC1 expression.
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Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, United States.
Rationale: CC16 (Club Cell Secretory Protein) is a protein produced by club cells and other non-ciliated epithelial cells within the lungs. CC16 has been shown to protect against the development of obstructive lung diseases and attenuate pulmonary pathogen burden. Despite recent advances in understanding CC16 effects in circulation, the biological mechanisms of CC16 in pulmonary epithelial responses have not been elucidated.
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