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PubMed:23659346 JSONTXT 43 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
TextSentencer_T1 0-122 Sentence denotes Integrative toxicoproteomics implicates impaired mitochondrial glutathione import as an off-target effect of troglitazone.
T1 0-122 Sentence denotes Integrative toxicoproteomics implicates impaired mitochondrial glutathione import as an off-target effect of troglitazone.
TextSentencer_T2 123-287 Sentence denotes Troglitazone, a first-generation thiazolidinedione of antihyperglycaemic properties, was withdrawn from the market due to unacceptable idiosyncratic hepatotoxicity.
T2 123-287 Sentence denotes Troglitazone, a first-generation thiazolidinedione of antihyperglycaemic properties, was withdrawn from the market due to unacceptable idiosyncratic hepatotoxicity.
TextSentencer_T3 288-396 Sentence denotes Despite intensive research, the underlying mechanism of troglitazone-induced liver toxicity remains unknown.
T3 288-396 Sentence denotes Despite intensive research, the underlying mechanism of troglitazone-induced liver toxicity remains unknown.
TextSentencer_T4 397-647 Sentence denotes Here we report the use of the Sod2(+/-) mouse model of silent mitochondrial oxidative-stress-based and quantitative mass spectrometry-based proteomics to track the mitochondrial proteome changes induced by physiologically relevant troglitazone doses.
T4 397-647 Sentence denotes Here we report the use of the Sod2(+/-) mouse model of silent mitochondrial oxidative-stress-based and quantitative mass spectrometry-based proteomics to track the mitochondrial proteome changes induced by physiologically relevant troglitazone doses.
TextSentencer_T5 648-872 Sentence denotes By quantitative untargeted proteomics, we first globally profiled the Sod2(+/-) hepatic mitochondria proteome and found perturbations including GSH metabolism that enhanced the toxicity of the normally nontoxic troglitazone.
T5 648-872 Sentence denotes By quantitative untargeted proteomics, we first globally profiled the Sod2(+/-) hepatic mitochondria proteome and found perturbations including GSH metabolism that enhanced the toxicity of the normally nontoxic troglitazone.
TextSentencer_T6 873-1266 Sentence denotes Short- and long-term troglitazone administration in Sod2(+/-) mouse led to a mitochondrial proteome shift from an early compensatory response to an eventual phase of intolerable oxidative stress, due to decreased mitochondrial glutathione (mGSH) import protein, decreased dicarboxylate ion carrier (DIC), and the specific activation of ASK1-JNK and FOXO3a with prolonged troglitazone exposure.
T6 873-1266 Sentence denotes Short- and long-term troglitazone administration in Sod2(+/-) mouse led to a mitochondrial proteome shift from an early compensatory response to an eventual phase of intolerable oxidative stress, due to decreased mitochondrial glutathione (mGSH) import protein, decreased dicarboxylate ion carrier (DIC), and the specific activation of ASK1-JNK and FOXO3a with prolonged troglitazone exposure.
TextSentencer_T7 1267-1518 Sentence denotes Furthermore, mapping of the detected proteins onto mouse specific protein-centered networks revealed lipid-associated proteins as contributors to overt mitochondrial and liver injury when under prolonged exposure to the lipid-normalizing troglitazone.
T7 1267-1518 Sentence denotes Furthermore, mapping of the detected proteins onto mouse specific protein-centered networks revealed lipid-associated proteins as contributors to overt mitochondrial and liver injury when under prolonged exposure to the lipid-normalizing troglitazone.
TextSentencer_T8 1519-1751 Sentence denotes By integrative toxicoproteomics, we demonstrated a powerful systems approach in identifying the collapse of specific fragile nodes and activation of crucial proteome reconfiguration regulators when targeted by an exogenous toxicant.
T8 1519-1751 Sentence denotes By integrative toxicoproteomics, we demonstrated a powerful systems approach in identifying the collapse of specific fragile nodes and activation of crucial proteome reconfiguration regulators when targeted by an exogenous toxicant.