O-GlcNAc Modification: Friend or Foe in Diabetic Cardiovascular Disease / 당뇨병
Korean Diabetes Journal
;
: 211-219, 2010.
Artículo
en Inglés
| WPRIM
| ID: wpr-48072
ABSTRACT
O-Linked beta-N-acetyl glucosaminylation (O-GlcNAcylation) is a dynamic post-translational modification that occurs on serine and threonine residues of cytosolic and nuclear proteins in all cell types, including those involved in the cardiovascular system. O-GlcNAcylation is thought to act in a manner analogous to protein phosphorylation. O-GlcNAcylation rapidly cycles on/off proteins in a time scale similar to that for phosphorylation/dephosphorylation of proteins. Several studies indicate that O-GlcNAc might induce nuclear localization of some transcription factors and may affect their DNA binding activities. However, at the cellular level, it has been shown that O-GlcNAc levels increase in response to stress and augmentation of this response suppresses cell survival. Increased levels of O-GlcNAc have been implicated as a pathogenic contributor to glucose toxicity and insulin resistance, which are major hallmarks of type 2 diabetes and diabetes-related cardiovascular complications. Thus, O-GlcNAc and its metabolic functions are not yet well-understood; focusing on the role of O-GlcNAc in the cardiovascular system is a viable target for biomedical investigation. In this review, we summarize our current understanding of the role of O-GlcNAc on the regulation of cell function and survival in the cardiovascular system.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Fosforilación
/
Acetilglucosaminidasa
/
Serina
/
Treonina
/
Factores de Transcripción
/
Enfermedades Vasculares
/
ADN
/
Resistencia a la Insulina
/
Proteínas Nucleares
/
Enfermedades Cardiovasculares
Límite:
Humanos
Idioma:
Inglés
Revista:
Korean Diabetes Journal
Año:
2010
Tipo del documento:
Artículo
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