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Artículo

Mitochondrial–nuclear communication by FKBP51 shuttling

Zgajnar, Nadia RominaIcon ; Lagadari, MarianaIcon ; Gallo, Luciana InesIcon ; Piwien Pilipuk, GracielaIcon ; Galigniana, Mario DanielIcon
Fecha de publicación: 02/2023
Editorial: Wiley-liss, div John Wiley & Sons Inc.
Revista: Journal of Cellular Biochemistry
ISSN: 0730-2312
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Bioquímica y Biología Molecular

Resumen

The HSP90-binding immunophilin FKBP51 is a soluble protein that shows high homology and structural similarity with FKBP52. Both immunophilins are functionally divergent and often show antagonistic actions. They were first described in steroid receptor complexes, their exchange in the complex being the earliest known event in steroid receptor activation upon ligand binding. In addition to steroid-related events, several pleiotropic actions of FKBP51 have emerged during the last years, ranging from cell differentiation and apoptosis to metabolic and psychiatric disorders. On the other hand, mitochondria play vital cellular roles in maintaining energy homeostasis, responding to stress conditions, and affecting cell cycle regulation, calcium signaling, redox homeostasis, and so forth. This is achieved by proteins that are encoded in both the nuclear genome and mitochondrial genes. This implies active nuclear-mitochondrial communication to maintain cell homeostasis. Such communication involves factors that regulate nuclear and mitochondrial gene expression affecting the synthesis and recruitment of mitochondrial and nonmitochondrial proteins, and/or changes in the functional state of the mitochondria itself, which enable mitochondria to recover from stress. FKBP51 has emerged as a serious candidate to participate in these regulatory roles since it has been unexpectedly found in mitochondria showing antiapoptotic effects. Such localization involves the tetratricopeptide repeats domains of the immunophilin and not its intrinsic enzymatic activity of peptidylprolyl-isomerase. Importantly, FKBP51 abandons the mitochondria and accumulates in the nucleus upon cell differentiation or during the onset of stress. Nuclear FKBP51 enhances the enzymatic activity of telomerase. The mitochondrial-nuclear trafficking is reversible, and certain situations such as viral infections promote the opposite trafficking, that is, FKBP51 abandons the nucleus and accumulates in mitochondria. In this article, we review the latest findings related to the mitochondrial-nuclear communication mediated by FKBP51 and speculate about the possible implications of this phenomenon.
Palabras clave: APOPTOSIS , CANCER , IMMUNOPHILIN , MITOCHONDRIA , SHUTTLING , STRESS
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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/216137
URL: https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.30386
DOI: http://dx.doi.org/10.1002/jcb.30386
Colecciones
Articulos(IBYME)
Articulos de INST.DE BIOLOGIA Y MEDICINA EXPERIMENTAL (I)
Citación
Zgajnar, Nadia Romina; Lagadari, Mariana; Gallo, Luciana Ines; Piwien Pilipuk, Graciela; Galigniana, Mario Daniel; Mitochondrial–nuclear communication by FKBP51 shuttling; Wiley-liss, div John Wiley & Sons Inc.; Journal of Cellular Biochemistry; 2-2023; 1-16
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