<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>2022</volume><submitter>Zhang Y</submitter><pubmed_abstract>Mitophagy and oxidative stress play important roles in Parkinson's disease (PD). Dysregulated mitophagy exacerbates mitochondrial oxidative damage; however, the regulatory mechanism of mitophagy is unclear. Here, we provide a potential mechanistic link between c-Abl, a nonreceptor tyrosine kinase, and mitophagy in PD progression. We found that c-Abl activation reduces the interaction of prohibitin 2 (PHB2) and microtubule-associated protein 1 light chain 3 (LC3) and decreases the expressive level of antioxidative stress proteins, including nuclear factor erythroid 2-related factor 2 (Nrf2), NADPH quinone oxidoreductase-1 (NQO-1), and the antioxidant enzyme heme oxygenase-1 (HO-1) in 1-methyl-4-phenylpyridinium- (MPP&lt;sup>+&lt;/sup>-) lesioned SH-SY5Y cells. Importantly, we found that MPP&lt;sup>+</pubmed_abstract><journal>Oxidative medicine and cellular longevity</journal><pagination>9233749</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9668474</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Nonreceptor Tyrosine Kinase c-Abl-Mediated PHB2 Phosphorylation Aggravates Mitophagy Disorder in Parkinson's Disease Model.</pubmed_title><pmcid>PMC9668474</pmcid><pubmed_authors>Shen M</pubmed_authors><pubmed_authors>Lai X</pubmed_authors><pubmed_authors>Wu J</pubmed_authors><pubmed_authors>Jin W</pubmed_authors><pubmed_authors>Yan J</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Yin S</pubmed_authors><pubmed_authors>Ma H</pubmed_authors><pubmed_authors>Sun D</pubmed_authors><pubmed_authors>Jiang M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Nonreceptor Tyrosine Kinase c-Abl-Mediated PHB2 Phosphorylation Aggravates Mitophagy Disorder in Parkinson's Disease Model.</name><description>Mitophagy and oxidative stress play important roles in Parkinson's disease (PD). Dysregulated mitophagy exacerbates mitochondrial oxidative damage; however, the regulatory mechanism of mitophagy is unclear. Here, we provide a potential mechanistic link between c-Abl, a nonreceptor tyrosine kinase, and mitophagy in PD progression. We found that c-Abl activation reduces the interaction of prohibitin 2 (PHB2) and microtubule-associated protein 1 light chain 3 (LC3) and decreases the expressive level of antioxidative stress proteins, including nuclear factor erythroid 2-related factor 2 (Nrf2), NADPH quinone oxidoreductase-1 (NQO-1), and the antioxidant enzyme heme oxygenase-1 (HO-1) in 1-methyl-4-phenylpyridinium- (MPP&lt;sup>+&lt;/sup>-) lesioned SH-SY5Y cells. Importantly, we found that MPP&lt;sup>+</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-21T14:23:01.626Z</modification><creation>2025-04-21T14:23:01.626Z</creation></dates><accession>S-EPMC9668474</accession><cross_references><pubmed>36406767</pubmed><doi>10.1155/2022/9233749</doi></cross_references></HashMap>