ArticleProceedings of the National Academy of Sciences of the United States of America2000
Identification of a renal-specific oxido-reductase in newborn diabetic mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 50 citations in OpenAlex.
- Myo-Inositol Oxygenase (MIOX): A Pivotal Regulator and Therapeutic Target in Multiple Diseases.Current issues in molecular biology · 2025Review
- MIOX inhibits autophagy to regulate the ROS -driven inhibition of STAT3/c-Myc-mediated epithelial-mesenchymal transition in clear cell renal cell carcinoma.Redox biology · 2023Article
- Excessively Enlarged Mitochondria in the Kidneys of Diabetic Nephropathy.Antioxidants (Basel, Switzerland) · 2021Review
- Myo-inositol oxygenase accentuates renal tubular injury initiated by endoplasmic reticulum stress.American journal of physiology. Renal physiology · 2019Article
- Nutritional and Acquired Deficiencies in Inositol Bioavailability. Correlations with Metabolic Disorders.International journal of molecular sciences · 2017Review
- Molecular cloning of the myo-inositol oxygenase gene from the kidney of baboons.Biomedical reports · 2017Article
- Beneficial Effects ofJournal of the American Society of Nephrology : JASN · 2017Article
- myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience: A NEW MECHANISM RELEVANT TO THE PATHOGENESIS OF DIABETIC NEPHROPATHY.The Journal of biological chemistry · 2016Article
- Transcriptional and Translational Modulation of myo-Inositol Oxygenase (Miox) by Fatty Acids: IMPLICATIONS IN RENAL TUBULAR INJURY INDUCED IN OBESITY AND DIABETES.The Journal of biological chemistry · 2016Article
- Disruption of renal tubular mitochondrial quality control by Myo-inositol oxygenase in diabetic kidney disease.Journal of the American Society of Nephrology : JASN · 2015Article
- Transcriptional and post-translational modulation of myo-inositol oxygenase by high glucose and related pathobiological stresses.The Journal of biological chemistry · 2011Article
- Discovery of genes related to diabetic nephropathy in various animal models by current techniques.Contributions to nephrology · 2011Article
- Pathobiology of renal-specific oxidoreductase/myo-inositol oxygenase in diabetic nephropathy: its implications in tubulointerstitial fibrosis.American journal of physiology. Renal physiology · 2010Article
- Historical chronology of basic and clinical research in diabetic nephropathy and contributions of Japanese scientists.Clinical and experimental nephrology · 2009Review
- Crystal structure of a substrate complex of myo-inositol oxygenase, a di-iron oxygenase with a key role in inositol metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Purification, crystallization and preliminary crystallographic analysis of mouse myo-inositol oxygenase.Acta crystallographica. Section F, Structural biology and crystallization communications · 2006Article
- Modulation of renal-specific oxidoreductase/myo-inositol oxygenase by high-glucose ambience.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Identification of adipocyte adhesion molecule (ACAM), a novel CTX gene family, implicated in adipocyte maturation and development of obesity.The Biochemical journal · 2005Article
- Renal tubule-specific expression and urinary secretion of human growth hormone: a kidney-based transgenic bioreactor growth.Transgenic research · 2003Article
- myo-Inositol oxygenase: molecular cloning and expression of a unique enzyme that oxidizes myo-inositol and D-chiro-inositol.The Biochemical journal · 2001Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Aldose reductase (ALR2), a NADPH-dependent aldo-keto reductase (AKR), is widely distributed in mammalian tissues and has been implicated in complications of diabetes, including diabetic nephropathy. To identify a renal-specific reductase belonging to the AKR family, representational difference analyses of cDNA from diabetic mouse kidney were performed. A full-length cDNA with an ORF of 855 nt and yielding a approximately 1.5-kb mRNA transcript was isolated from a mouse kidney library. Human and rat homologues also were isolated, and they had approximately 91% and approximately 97% amino acid identity with mouse protein. In vitro translation of the cDNA yielded a protein product of approximately 33 kDa. Northern and Western blot analyses, using the cDNA and antirecombinant protein antibody, revealed its expression exclusively confined to the kidney. Like ALR2, the expression was up-regulated in diabetic kidneys. Its mRNA and protein expression was restricted to renal proximal tubules. The gene neither codistributed with Tamm-Horsfall protein nor aquaporin-2. The deduced protein sequence revealed an AKR-3 motif located near the N terminus, unlike the other AKR family members where it is confined to the C terminus. Fluorescence quenching and reactive blue agarose chromatography studies revealed that it binds to NADPH with high affinity (K(dNADPH) = 66.9 +/- 2.3 nM). This binding domain is a tetrapeptide (Met-Ala-Lys-Ser) located within the AKR-3 motif that is similar to the other AKR members. The identified protein is designated as RSOR because it is renal-specific with properties of an oxido-reductase, and like ALR2 it may be relevant in the renal complications of diabetes mellitus.
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