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| http://dx.doi.org/10.1016/j.ajhg.2025.08.001 | DOI Listing |
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Nfe2l1 dysfunction alters Parkinson's disease-related gene expression and impairs neuronal differentiation under ubiquitin stress in neuronal differentiated P19 Cells.
Sci Rep
August 2025
Department of Experimental Embryology, Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences, Postępu 36, 05-552, Jastrzebiec, Poland.
Proteostasis is essential for neuronal health, and its disruption is implicated in neurodegenerative diseases such as Parkinson's disease (PD). Nfe2l1, a key regulator of proteostasis and ubiquitination, plays a significant role in neuronal health, yet its molecular functions in neuronal cells remain unclear. Our study investigates the role of Nfe2l1 in RA-induced neuronal differentiation of P19 cells under proteasome inhibition.
View Article and Find Full Text PDFCardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.
Am J Physiol Heart Circ Physiol
September 2025
Department of Pharmacology, University of California San Diego School of Medicine, La Jolla, California, United States.
Cardiomyocyte signaling through the transcriptional coactivator Yes-associated protein (YAP) has been shown to protect the myocardium against ischemic or mechanical stress. Inflammatory responses initiated in cardiomyocytes play a major role in the development of cardiac dysfunction. We tested the relationship between YAP and inflammatory gene expression using cardiomyocyte-specific YAP-knockout (KO) mice.
View Article and Find Full Text PDFRNA Helicase DDX5 Maintains Cardiac Function by Regulating Alternative Splicing.
Circulation
October 2024
Department of Cardiovascular Medicine, Ruijin Hospital (K.J., H.C., W.M., L.Z., Z.L., Z.W., H.S., Y.C., H.Z., H.X., L.Y., Z.C., L.L., R.Z., X.Y.), School of Medicine, Shanghai Jiao Tong University, China.
Background: Heart failure (HF) is a leading cause of morbidity and mortality worldwide. RNA-binding proteins are identified as regulators of cardiac disease; DDX5 (dead-box helicase 5) is a master regulator of many RNA processes, although its function in heart physiology remains unclear.
Methods: We assessed DDX5 expression in human failing hearts and a mouse HF model.
Nitric oxide contributes to rapid sclerostin protein loss following mechanical load.
Biochem Biophys Res Commun
October 2024
Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA. Electronic address:
In response to mechanical loading of bone, osteocytes produce nitric oxide (NO•) and decrease sclerostin protein expression, leading to an increase in bone mass. However, it is unclear whether NO• production and sclerostin protein loss are mechanistically linked, and, if so, the nature of their hierarchical relationship within an established mechano-transduction pathway. Prior work showed that following fluid-shear stress (FSS), osteocytes produce NOX2-derived reactive oxygen species, inducing calcium (Ca) influx.
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