SIRT1 promotes endothelium-dependent vascular relaxation by activating endothelial nitric oxide synthase
By I. Mattagajasingh, Cuk-Seong Kim, Asma Naqvi, T. Yamamori, T. A. Hoffman, Saet-Byel Jung, Jeremy Dericco, K. Kasuno, K. Irani. Proceedings of the National Academy of Sciences of the United States of America, 2007
867 citations recorded by the source corpus.
Subfields: Biochemistry, Endocrine and Autonomic Systems, Geriatrics and Gerontology
View Paper: https://www.semanticscholar.org/paper/daf5b1d7f39e4a3b7b44158ea7c1a73d238f1c0c
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In Biochemistry
In Endocrine and Autonomic Systems
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Citations in the corpus
- SIRT1 and other sirtuins in Metabolism (2013, background): “Interestingly, SIRT1 and eNOS form a positive regulatory loop: upon CR, eNOS induces SIRT1 expression and, SIRT1 further promotes eNOS activity through deacetylation [85].”
- Endothelial dysfunction and vascular disease – a 30th anniversary update (2017, background): “The favourable effect of caloric restriction on endothelium-dependent, NO-mediated relaxations can be attributed to the deacetylation and activation of eNOS by SIRT1 (Mattagajasingh et al. 2007).”
- Lysine acetylation: codified crosstalk with other posttranslational modifications (2008, background): “For example, acetylation of acetyl-CoA synthase (Starai et al., 2002) and nitric oxide synthase (Mattagajasingh et al., 2007) inactivates the enzymes, whereas a-tubulin acetylation (Figure 6A) generates a simple mark for cargo transport.”
- Resources and Biological Activities of Natural Polyphenols (2014, background): “SIRT1 was known to regulate the activity of several important transcription factors and coactivators that are essential for the protection of numerous types of cardiovascular disturbances, such as Forkhead box O, NO production, Hif-2α [67–69].”