{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Krug AK"],"funding":["NIEHS NIH HHS","FDA HHS"],"pagination":["e1222"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4047858"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5"],"pubmed_abstract":["Assessment of the network of toxicity pathways by Omics technologies and bioinformatic data processing paves the road toward a new toxicology for the twenty-first century. Especially, the upstream network of responses, taking place in toxicant-treated cells before a point of no return is reached, is still little explored. We studied the effects of the model neurotoxicant 1-methyl-4-phenylpyridinium (MPP(+)) by a combined metabolomics (mass spectrometry) and transcriptomics (microarrays and deep sequencing) approach to provide unbiased data on earliest cellular adaptations to stress. Neural precursor cells (LUHMES) were differentiated to homogeneous cultures of fully postmitotic human dopaminergic neurons, and then exposed to the mitochondrial respiratory chain inhibitor MPP(+) (5 μM). At 1"],"journal":["Cell death & disease"],"pubmed_title":["Transcriptional and metabolic adaptation of human neurons to the mitochondrial toxicant MPP(+)."],"pmcid":["PMC4047858"],"funding_grant_id":["R01ES020750","U01FD004230","R01 ES020750","U01 FD004230"],"pubmed_authors":["Jagtap S","Sachinidis A","Gutbier S","Forster S","Ivanova V","Schildknecht S","Adam M","Hartung T","Krug AK","Poltl D","Leist M","Brunner T","Zhao L","Kullmann C","Hiller K","Farhan H","Meiser J","Leparc G"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptional and metabolic adaptation of human neurons to the mitochondrial toxicant MPP(+).","description":"Assessment of the network of toxicity pathways by Omics technologies and bioinformatic data processing paves the road toward a new toxicology for the twenty-first century. Especially, the upstream network of responses, taking place in toxicant-treated cells before a point of no return is reached, is still little explored. We studied the effects of the model neurotoxicant 1-methyl-4-phenylpyridinium (MPP(+)) by a combined metabolomics (mass spectrometry) and transcriptomics (microarrays and deep sequencing) approach to provide unbiased data on earliest cellular adaptations to stress. Neural precursor cells (LUHMES) were differentiated to homogeneous cultures of fully postmitotic human dopaminergic neurons, and then exposed to the mitochondrial respiratory chain inhibitor MPP(+) (5 μM). At 1","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 May","modification":"2026-05-04T22:41:59.994Z","creation":"2019-03-27T01:29:36Z"},"accession":"S-EPMC4047858","cross_references":{"pubmed":["24810058"],"doi":["10.1038/cddis.2014.166"]}}