[Figure: see text].
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http://dx.doi.org/10.1161/CIRCRESAHA.119.316547 | DOI Listing |
Unlabelled: Z-lines are core ultrastructural organizers of cardiomyocytes that modulate many facets of cardiac pathogenesis. Yet a comprehensive proteomic atlas of Z-line-associated components remain incomplete. Here, we established an adeno-associated virus (AAV)-delivered, cardiomyocyte-specific, proximity-labeling approach to characterize the Z-line proteome in vivo.
View Article and Find Full Text PDFActa Neuropathol Commun
April 2022
School of Biomedical Sciences, The University of Queensland, St. Lucia, QLD, 4072, Australia.
A central event in the pathogenesis of motor neuron disease (MND) is the loss of neuromuscular junctions (NMJs), yet the mechanisms that lead to this event in MND remain to be fully elucidated. Maintenance of the NMJ relies upon neural agrin (n-agrin) which, when released from the nerve terminal, activates the postsynaptic Muscle Specific Kinase (MuSK) signaling complex to stabilize clusters of acetylcholine receptors. Here, we report that muscle from MND patients has an increased proportion of slow fibers and muscle fibers with smaller diameter.
View Article and Find Full Text PDFJ Cell Biol
December 2021
Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland, Australia.
The cavin proteins are essential for caveola biogenesis and function. Here, we identify a role for the muscle-specific component, Cavin4, in skeletal muscle T-tubule development by analyzing two vertebrate systems, mouse and zebrafish. In both models, Cavin4 localized to T-tubules, and loss of Cavin4 resulted in aberrant T-tubule maturation.
View Article and Find Full Text PDFCirc Res
March 2021
Cellular Biophysics and Translational Cardiology Section, Heart Research Center Göttingen (J.P., D.K.-D., G.W., S.B., T.K., G.H., J.W., S.E.L.), University Medical Center Göttingen.
[Figure: see text].
View Article and Find Full Text PDFJ Mol Cell Cardiol
April 2021
Jiangxi Key Laboratory of Molecular Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China; Department of Cardiovascular Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China. Electronic address:
Autophagy plays a deleterious role in ischemic myocardial injury. The deacetylase SIRT1 is a well-established regulator of autophagy that can be modified by the ubiquitin-like protein SUMO1. Our previous work demonstrated that another ubiquitin-like protein, FAT10, exerts cardioprotective effects against myocardial ischemia by stabilizing the caveolin-3 protein; however, the effects of FAT10 on autophagy through SIRT1 are unclear.
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