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Noncanonical role of Golgi-associated macrophage TAZ in chronic inflammation and tumorigenesis.
Sci Adv
January 2025
Department of Biochemistry, College of Life Science and Biotechnology, Brain Korea 21 Project, Yonsei University, Seoul 03722, Republic of Korea.
Until now, Hippo pathway-mediated nucleocytoplasmic translocation has been considered the primary mechanism by which yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) transcriptional coactivators regulate cell proliferation and differentiation via transcriptional enhanced associate domain (TEAD)-mediated target gene expression. In this study, however, we found that TAZ, but not YAP, is associated with the Golgi apparatus in macrophages activated via Toll-like receptor ligands during the resolution phase of inflammation. Golgi-associated TAZ enhanced vesicle trafficking and secretion of proinflammatory cytokines in M1 macrophage independent of the Hippo pathway.
View Article and Find Full Text PDFAMPA Receptors in Synaptic Plasticity, Memory Function, and Brain Diseases.
Cell Mol Neurobiol
January 2025
Laboratory of Neurobiology, Centro de Investigaciones Medico Sanitarias (CIMES), University of Malaga, Calle Marqués de Beccaria, 3, Campus Teatinos s/n, 29010, Malaga, Spain.
Tetrameric AMPA-type ionotropic glutamate receptors are primary transducers of fast excitatory synaptic transmission in the central nervous system, and their properties and abundance at the synaptic surface are crucial determinants of synaptic efficacy in neuronal communication across the brain. The induction of long-term potentiation (LTP) leads to the insertion of GluA1-containing AMPA receptors at the synaptic surface, whereas during long-term depression (LTD), these receptors are internalized into the cytoplasm of the spine. Disruptions in the trafficking of AMPA receptors to and from the synaptic surface attenuate both forms of synaptic plasticity.
View Article and Find Full Text PDFMyelodysplastic syndromes (MDS) are age-related diseases characterized by bone marrow (BM) dysfunction and an increased risk of developing acute leukemia. While there is growing evidence highlighting the crucial role of the BM microenvironment (BMME) in MDS, the specific influence of inflammation on BMME changes, as well as the potential benefits of targeting cytokines therapeutically, remain to be elucidated. We previously found interleukin-1 (IL-1) to be a driver of aging phenotypes of BMME and hematopoietic stem and progenitor cells (HSPCs).
View Article and Find Full Text PDFHandgrip strength measurement protocols in individuals with Down syndrome: a systematic review and meta-regression.
Ann Med
December 2025
Health Research and Innovatioin Science Centre, Klaipeda University, Klaipeda, Lithuania.
Background: Handgrip strength (HGS) serves as a robust predictor of overall strength across various populations, including individuals with Down Syndrome (DS).
Objective: To analyze the HGS measurement protocols used in studies involving individuals with DS.
Methods: Primary sources were sourced from six databases: PubMed, Scopus, Ovid, Embase, ERIC, and Web of Science, spanning from inception to 23rd December 2023.
The PKM2 activator TEPP-46 suppresses cellular senescence in hydrogen peroxide-induced proximal tubular cells and kidney fibrosis in CD-1 mice.
J Diabetes Investig
January 2025
Faculty of Medicine, Internal Medicine, Shimane University, Izumo, Shimane, Japan.
Aim/introduction: Senescence is a key driver of age-related kidney dysfunction, including diabetic kidney disease. Oxidative stress activates cellular senescence, induces abnormal glycolysis, and is associated with pyruvate kinase muscle isoform 2 (PKM2) dysfunction; however, the mechanisms linking PK activation to cellular senescence have not been elucidated. We hypothesized that PKM2 activation by TEPP-46 could suppress oxidative stress-induced renal tubular cell injury and cellular senescence.
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