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The Journal of Clinical Investigation|March 1, 1992
Beta-adrenergic neuroeffector abnormalities in the failing human heart are produced by local rather than systemic mechanismsM R Bristow, W Minobe, R Rasmussen, et al.
Italian Heart Journal : Official Journal of the Italian Federation of Cardiology|May 26, 2001
Current perspective new insights into the molecular basis of familial dilated cardiomyopathyG Sinagra, A Di Lenarda, G L Brodsky, et al.
British Heart Journal|February 1, 1993
Familial aggregation of idiopathic dilated cardiomyopathy: clinical features and pedigree analysis in 14 familiesE Zachara, A L Caforio, G P Carboni, et al.
Molecular & Cellular Proteomics : MCP|March 15, 2021
Quantitative Proteomics Reveals that the OGT Interactome Is Remodeled in Response to Oxidative StressMarissa Martinez, Santosh Renuse, Simion Kreimer, et al.
Human Molecular Genetics|January 1, 1996
A point mutation in the 5' splice site of the dystrophin gene first intron responsible for X-linked dilated cardiomyopathyJ Milasin, F Muntoni, G M Severini, et al.
Proteomics|September 30, 2014
Quantitative phosphoproteomics reveals crosstalk between phosphorylation and O-GlcNAc in the DNA damage response pathwayJun Zhong, Marissa Martinez, Srona Sengupta, et al.
The Journal of Biological Chemistry|October 16, 2025
Loss of O-GlcNAcylation in cardiac myocytes triggers the integrated stress response, contributing to heart failureKyriakos N Papanicolaou, Wenxi Zhang, Aidan J Dunphy, et al.
Proceedings of the National Academy of Sciences of the United States of America|January 9, 2021
Mammalian cell proliferation requires noncatalytic functions of O-GlcNAc transferaseZebulon G Levine, Sarah C Potter, Cassandra M Joiner, et al.
Analytical Biochemistry|July 28, 2023
Differential Detection of O-GlcNAcylated proteins in the heart using antibodiesBhargavi Narayanan, Fiddia Zahra, Russell A Reeves, et al.
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