PARKIN is not required to sustain OXPHOS function in adult mammalian tissues

• Published in: NPJ Parkinson's Disease Vol. 10; no. 1; pp. 93 - 14
• Main Authors: Filograna, Roberta, Gerlach, Jule, Choi, Hae-Na, Rigoni, Giovanni, Barbaro, Michela, Oscarson, Mikael, Lee, Seungmin, Tiklova, Katarina, Ringnér, Markus, Koolmeister, Camilla, Wibom, Rolf, Riggare, Sara, Nennesmo, Inger, Perlmann, Thomas, Wredenberg, Anna, Wedell, Anna, Motori, Elisa, Svenningsson, Per, Larsson, Nils-Göran
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 29.04.2024; Nature Publishing Group; Nature Portfolio
• Subjects: 631/337; 631/378/1689/1718; Basic Medicine; Bioinformatics and Computational Biology; Bioinformatics and Systems Biology; Bioinformatik och beräkningsbiologi; Bioinformatik och systembiologi; Biologi; Biological Sciences; Biomedical and Life Sciences; Biomedicine; Medical and Health Sciences; Medical Science; Medicin och hälsovetenskap; Medicinsk vetenskap; Medicinska och farmaceutiska grundvetenskaper; Mitochondrial DNA; Musculoskeletal system; Natural Sciences; Naturvetenskap; Neurology; Neurosciences; Neurovetenskaper

Loss-of-function variants in the PRKN gene encoding the ubiquitin E3 ligase PARKIN cause autosomal recessive early-onset Parkinson’s disease (PD). Extensive in vitro and in vivo studies have reported that PARKIN is involved in multiple pathways of mitochondrial quality control, including mitochondri...