M
Mineko Terao
Researcher at Mario Negri Institute for Pharmacological Research
Publications - 125
Citations - 5095
Mineko Terao is an academic researcher from Mario Negri Institute for Pharmacological Research. The author has contributed to research in topics: Retinoic acid & Aldehyde oxidase. The author has an hindex of 44, co-authored 119 publications receiving 4738 citations. Previous affiliations of Mineko Terao include University of Ferrara & Laboratory of Molecular Biology.
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Mammalian molybdo-flavoenzymes, an expanding family of proteins: structure, genetics, regulation, function and pathophysiology
TL;DR: Current knowledge on the structure, enzymology, genetics, regulation and pathophysiology of mammalian molybdo-flavoenzymes is summarized.
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Mammalian aldehyde oxidases: genetics, evolution and biochemistry
TL;DR: An overview of the current knowledge of genetics, evolution, structure, enzymology, tissue distribution and regulation of mammalian aldehyde oxidases is provided.
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The role of aldehyde oxidase in drug metabolism
Enrico Garattini,Mineko Terao +1 more
TL;DR: There is evidence for an increasing relevance of AOX1 in the metabolism and clearance of new drugs, as measures aiming at controlling CYP450-dependent metabolism of prospective therapeutic agents are becoming routine.
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Cytokine induction of haem oxygenase mRNA in mouse liver. Interleukin 1 transcriptionally activates the haem oxygenase gene.
TL;DR: Results indicate that enzymic haem catabolism in the liver is a process inducible in vivo by inflammatory cytokines, which up-regulate HO synthesis at the transcriptional level.
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Stat1 Is Induced and Activated by All-Trans Retinoic Acid in Acute Promyelocytic Leukemia Cells
Maurizio Gianni,Mineko Terao,Ida Fortino,Marco Li-Calzi,Vincenzo Viggiano,Tiziano Barbui,Alessandro Rambaldi,Enrico Garattini +7 more
TL;DR: The data show that ATRA is capable of modulating the amounts and the state of activation of some of the components of the IFN intracellular signaling pathways, and suggest that the retinoid can bypass IFN/IFN-receptor interactions and induce the expression of IFN-regulated genes.