Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/15738
Título
Targeting ERK3/MK5 complex for treatment of obesity and diabetes.
Autor(es)
Fecha de publicación
2022-07-05
Cita
Biochem Biophys Res Commun. 2022 Jul 5;612:119-125
Idioma
Inglés
Tipo de documento
journal article
Resumen
Kinases represent one of the largest druggable families of proteins. Importantly, many kinases are aberrantly activated/de-activated in multiple organs during obesity, which contributes to the development of diabetes and associated diseases. Previous results indicate that the complex between Extracellular-regulated kinase 3 (ERK3) and Mitogen-Activated Protein Kinase (MAPK)-activated protein kinase 5 (MK5) suppresses energy dissipation and promotes fatty acids (FAs) output in adipose tissue and, therefore promotes obesity and diabetes. However, the therapeutic potential of targeting this complex at the systemic level has not been fully explored. Here we applied a translational approach to target the ERK3/MK5 complex in mice. Importantly, deletion of ERK3 in the whole body or administration of MK5-specific inhibitor protects against obesity and promotes insulin sensitivity. Finally, we show that the expression of ERK3 and MK5 correlates with the degree of obesity and that ERK3/MK5 complex regulates energy dissipation in human adipocytes. Altogether, we demonstrate that ERK3/MK5 complex can be targeted in vivo to preserve metabolic health and combat obesity and diabetes.
MESH
Diabetes Mellitus | Protein Serine-Threonine Kinases | Animals | Intracellular Signaling Peptides and Proteins | Mice | Mitogen-Activated Protein Kinase 6 | Obesity
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DOI
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