Isocitrate protects DJ-1 null dopaminergic cells from oxidative stress through NADP+-dependent isocitrate dehydrogenase (IDH)
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{"title"=>"Isocitrate protects DJ-1 null dopaminergic cells from oxidative stress through NADP+-dependent isocitrate dehydrogenase (IDH)", "type"=>"journal", "authors"=>[{"first_name"=>"Jinsung", "last_name"=>"Yang", "scopus_author_id"=>"57131791200"}, {"first_name"=>"Min Ju", "last_name"=>"Kim", "scopus_author_id"=>"57131561300"}, {"first_name"=>"Woongchang", "last_name"=>"Yoon", "scopus_author_id"=>"57195565149"}, {"first_name"=>"Eun Young", "last_name"=>"Kim", "scopus_author_id"=>"57195569182"}, {"first_name"=>"Hyunjin", "last_name"=>"Kim", "scopus_author_id"=>"56996355800"}, {"first_name"=>"Yoonjeong", "last_name"=>"Lee", "scopus_author_id"=>"34872586800"}, {"first_name"=>"Boram", "last_name"=>"Min", "scopus_author_id"=>"57195565897"}, {"first_name"=>"Kyung Shin", "last_name"=>"Kang", "scopus_author_id"=>"57195562059"}, {"first_name"=>"Jin H.", "last_name"=>"Son", "scopus_author_id"=>"57194693252"}, {"first_name"=>"Hwan Tae", "last_name"=>"Park", "scopus_author_id"=>"12754817400"}, {"first_name"=>"Jongkyeong", "last_name"=>"Chung", "scopus_author_id"=>"56040953500"}, {"first_name"=>"Hyongjong", "last_name"=>"Koh", "scopus_author_id"=>"7202301030"}], "year"=>2017, "source"=>"PLoS Genetics", "identifiers"=>{"pui"=>"618201487", "sgr"=>"85028806689", "issn"=>"15537404", "pmid"=>"28827794", "scopus"=>"2-s2.0-85028806689", "doi"=>"10.1371/journal.pgen.1006975"}, "id"=>"f5b300df-3895-3f9e-94fe-a5c7fa5e452a", "abstract"=>"DJ-1 is one of the causative genes for early onset familiar Parkinson's disease (PD) and is also considered to influence the pathogenesis of sporadic PD. DJ-1 has various physiological functions which converge on controlling intracellular reactive oxygen species (ROS) levels. In RNA-sequencing analyses searching for novel anti-oxidant genes downstream of DJ-1, a gene encoding NADP+-dependent isocitrate dehydrogenase (IDH), which converts isocitrate into alpha-ketoglutarate, was detected. Loss of IDH induced hyper-sensitivity to oxidative stress accompanying age-dependent mitochondrial defects and dopaminergic (DA) neuron degeneration in Drosophila, indicating its critical roles in maintaining mitochondrial integrity and DA neuron survival. Further genetic analysis suggested that DJ-1 controls IDH gene expression through nuclear factor-E2-related factor2 (Nrf2). Using Drosophila and mammalian DA models, we found that IDH suppresses intracellular and mitochondrial ROS level and subsequent DA neuron loss downstream of DJ-1. Consistently, trimethyl isocitrate (TIC), a cell permeable isocitrate, protected mammalian DJ-1 null DA cells from oxidative stress in an IDH-dependent manner. These results suggest that isocitrate and its derivatives are novel treatments for PD associated with DJ-1 dysfunction.", "link"=>"http://www.mendeley.com/research/isocitrate-protects-dj1-null-dopaminergic-cells-oxidative-stress-through-nadpdependent-isocitrate-de", "reader_count"=>6, "reader_count_by_academic_status"=>{"Student > Doctoral Student"=>1, "Student > Bachelor"=>2, "Lecturer"=>1, "Student > Ph. D. Student"=>1, "Professor > Associate Professor"=>1}, "reader_count_by_user_role"=>{"Student > Doctoral Student"=>1, "Student > Bachelor"=>2, "Lecturer"=>1, "Student > Ph. D. Student"=>1, "Professor > Associate Professor"=>1}, "reader_count_by_subject_area"=>{"Engineering"=>1, "Biochemistry, Genetics and Molecular Biology"=>2, "Agricultural and Biological Sciences"=>1, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Computer Science"=>1}, "reader_count_by_subdiscipline"=>{"Engineering"=>{"Engineering"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>1}, "Computer Science"=>{"Computer Science"=>1}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>2}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "group_count"=>0}

Scopus | Further Information

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