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FLASH GENE

Symbol

MIOX

contributors: mct/npt - updated : 15-04-2020

HGNC name	myo-inositol oxygenase
HGNC id	14522

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

DNA

TYPE	functioning gene
STRUCTURE	6.66 kb     10 Exon(s)

regulatory sequence	Promoter
	cytosine-phosphate-guanine/HTF
	Binding site   transcription factor   HRE
text structure	an osmotic response element (ORE) in the promoter region, which is present approximately 2 kb upstream of the translation start sit
	activity of the promoter is dependent on the binding of the transcription factor, tonicity element-binding protein, or osmotic response element-binding protein, to the ORE site
	MIOX promoters, enriched with CpG sites, are hypomethylated and unmethylated under high glucose (HG) ambience and hyperglycemic states associated with increased MIOX expression
	promoter includes oxidant-response elements, and binding sites for XBP1, a transcription factor of ER stress response

MAPPING

cloned

Y

linked

N

status

provisional

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_017584 10 - 1689 NP_060054 33 285 - 2017 28208054

EXPRESSION

Type

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Reproductive male system prostate       Urinary kidney tubule convoluted tubule proximal tubule highly Homo sapiens

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains

HOMOLOGY

interspecies	homolog to murine Aldrl6
	homolog to Drosophila mRpS7

Homologene

FAMILY

myo-inositol oxygenase family

CATEGORY

enzyme

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,cytoplasm,cytosolic

basic FUNCTION	non-heme iron enzyme, catalyzing the oxidative cleavage of myo-inositol to give D-glucuronic acid, a committed step in myo-inositol catabolism
	MIOX catalyzes the oxidative cleavage of myo-inositol (MI) to give D-glucuronic acid, a committed step in MI catabolism
	tubular-specific enzyme, modulating redox imbalance and apoptosis in tubular cells in diabetes
	epigenetic regulation of MIOX in the pathogenesis of diabetic tubulopathy
	MIOX expression profile modulates pathogenic ferroptosis in the renal proximal tubule

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

carbohydrate

signaling

myo-inositol catabolism pathway

a component

INTERACTION

DNA

RNA

small molecule

protein

high fat diet (HFD) or fatty acids modulate transcriptional, translational, and post-translational regulation of MIOX expression/activity and underscore MIOX being a novel target of the transcription factor SREBF1

cell & other

REGULATION

activated by

a positive feedback mechanism where xylitol, one of the products of myo-inositol catabolism via the glucuronate-xylulose pathway, induces an overexpression of MIOX

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional     --over   drives the progression of renal tubulo-interstitial injury in diabetes constitutional     --over   in diabetic kidneys may contribute to tubulointerstitial injury and the development of diabetic nephropathy

Susceptibility

to Type 1 diabetes mellitus

Variant & Polymorphism other	polymorphism (rs761745) in the promoter region of MIOX gene may be associated with the development of T1D

Candidate gene
Marker	MIOX levels were higher in gestational diabetes mellitus (GDM) cases so, it may be have a role in myo-inositol catabolism
	potential use of MIOX as a kidney-specific enzyme in the early diagnosis of acute kidney injury (AKI)
	concentration of MIOX in the serum and urine may serve as a new biomarker for the early diagnosis of diabetic nephropathy (DN)
Therapy target

ANIMAL & CELL MODELS

	expression of MIOX was increased at both the mRNA and protein levels in the kidney of rats with diabetic nephropathy
	in tubules of diabetic mice, increased MIOX expression and mitochondrial fragmentation and defective autophagy were observed