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Ronald J. Holewinski

Researcher at Cedars-Sinai Medical Center

Publications -  39
Citations -  1113

Ronald J. Holewinski is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Phosphorylation & Heart failure. The author has an hindex of 16, co-authored 36 publications receiving 825 citations. Previous affiliations of Ronald J. Holewinski include Johns Hopkins University School of Medicine & Johns Hopkins University.

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PKG1-modified TSC2 regulates mTORC1 activity to counter adverse cardiac stress

TL;DR: It is shown that phosphorylation or gain- or loss-of-function mutations at either of two adjacent serine residues in TSC2 can bidirectionally control mTORC1 activity stimulated by growth factors or haemodynamic stress, and consequently modulate cell growth and autophagy.
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Cardiac resynchronization sensitizes the sarcomere to calcium by reactivating GSK-3β

TL;DR: Data indicate that CRT improves calcium responsiveness of myofilaments following HF(dys) through GSK-3β reactivation, identifying a therapeutic approach to enhancing contractile function.
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Protein kinase A-dependent phosphorylation stimulates the transcriptional activity of hypoxia-inducible factor 1.

TL;DR: In this article, protein kinase A (PKA) was shown to activate the transcription of genes encoding proteins that enable cells to adapt to reduced O 2 availability, which contributes to the pathophysiology of cancer and heart disease.
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Characterization of the cardiac myosin binding protein-C phosphoproteome in healthy and failing human hearts

TL;DR: The most highly phosphorylated site on cMyBP-C was Ser284 and this site showed decreased phosphorylation in the failing heart, which implicates importance for fine-tuning contractility.