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Cell Death Discov. 2018 Feb 14;4:25. doi: 10.1038/s41420-018-0028-7. eCollection 2018 Dec.

GRK2 moderates the acute mitochondrial damage to ionizing radiation exposure by promoting mitochondrial fission/fusion.

Author information

1
1Department of Advanced Biomedical Sciences, "Federico II" University, Naples, Italy.
2
2Center for Pharmacogenomics, Washington University in St. Louis, St Louis, USA.
3
3Department of Medicine, Surgery and Dentistry, University of Salerno, Baronissi, Italy.
4
4Department of Translational Medical Sciences, "Federico II" University, Naples, Italy.
5
5Department of Molecular Medicine and Medical Biotechnologies "Federico II" University, Naples and Institute of Experimental Endocrinology and Oncology (IEOS-CNR), Naples, Italy.

Abstract

The modern understanding of the G protein-coupled receptor kinase 2 has grown towards the definition of a stress protein, for its ability to rapidly compartmentalize within the cell in response to acute stimulation. Also, mitochondria can be regulated by GRK2 localization. We show that Ionizing Radiation (IR) exposure acutely damages mitochondria regarding mass, morphology, and respiration, with recovery in a framework of hours. This phenomenon is actively regulated by GRK2, whose overexpression results to be protective, and reciprocally, deletion accelerates degenerative processes. The regulatory effects of the kinase involve a new interactome that includes binding HSP90 and binding and phosphorylation of the key molecules involved in the process of mitochondrial fusion and recovery: MFN-1 and 2.

Conflict of interest statement

The authors declare that they have no competing interests.

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