Ask about this productRelated genes to: MIOX antibody
- Gene:
- MIOX NIH gene
- Name:
- myo-inositol oxygenase
- Previous symbol:
- ALDRL6
- Synonyms:
- -
- Chromosome:
- 22q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-06
- Date modifiied:
- 2018-03-06
Related products to: MIOX antibody
Related articles to: MIOX antibody
- Myo-inositol (MI) plays key roles in cellular signaling, membrane structure, and metabolic regulation, with its effects in poultry primarily explored through direct dietary MI supplementation. In this study, we aimed to assess the effects of MI administration on post-hatch performance and metabolism of broiler chickens. A total of 480 fertilized Ross 308 eggs were divided into four groups and, on day 17 of incubation, were injected with 12 μmol/mL MI (MI 12), 24 μmol/mL MI (MI 24), 0.9% saline (positive control, PC), or left non-injected (negative control, NC). After hatching, broilers were group-housed in floor pens (8 pens per treatment), with 12 birds per pen, and fed a standard diet for 35 days. At d 35, one bird per pen was slaughtered, sex was identified, and blood and tissues were collected to assess MI concentrations, the expression of inositol monophosphatase 1 (IMPase 1) and myo-inositol oxygenase (MIOX), and plasma metabolite profiles. There was no adverse effect of MI administration on hatchability and body weight (BW) of hatchlings. During the growing period, BW was lower in MI-injected groups from day 14 onward, along with reduced average daily weight gain; however, no differences were observed in the feed conversion ratio. The survival rate was higher in MI-injected groups during days 0-21, with a positive trend until the end of the experiment. MI concentrations in plasma and tissues, along with the expression of IMPase 1 and MIOX, were not altered by treatment. Plasma metabolomics revealed higher C2 and C9 acylcarnitines, threonine, and sarcosine, along with lower serotonin, and notable changes in phosphatidylcholines and sphingolipids in MI-injected versus no-MI groups, potentially reflecting alterations in mitochondrial β-oxidation pathways, diacylglycerol-associated signaling, amino-acid-related metabolism, and peripheral serotonin metabolism. Sex-specific differences in plasma MI and metabolite profiles were detected, with male birds demonstrating reduced plasma MI concentrations, Fisher ratio, and carnosine levels, indicative of a metabolic state possibly associated with higher anabolic pressure or subclinical inflammatory activation. These findings highlight the potential of MI administration to induce subtle but persistent metabolic reprogramming and underscore the need for further studies to clarify its long-term consequences for metabolic resilience and performance in both sexes. - Source: PubMed
Publication date: 2026/02/09
Shomina NataliiaSommerfeld VeraRodehutscord MarkusHuber Korinna - Ferritinophagy is a selective form of macroautophagy/autophagy that mediates the degradation of ferritin complexes, releasing stored iron, and maintaining intracellular iron homeostasis. Proper regulation of ferritinophagy is essential for cellular adaptation to metabolic stress, whereas dysregulation disrupts iron balance and contributes to pathological processes. Excessive ferritinophagy leads to iron overload and reactive oxygen species accumulation, driving oxidative stress, ferroptosis, and inflammation, which are key contributors to cellular injury and progressive organ dysfunction. Despite advances in our understanding of autophagy and ferroptosis, the specific role of ferritinophagy in organ-specific injury remains unclear. In this review, we provide a comprehensive overview of the molecular mechanisms of ferritinophagy and critically examine its emerging roles in the pathogenesis of injuries to the heart, liver, lungs, and kidneys. We further highlight the therapeutic potential of targeting ferritinophagy and propose future research directions aimed at harnessing this pathway for the treatment of organ injuries. 3-MA: 3-methyladenine; ACO1/IRP1: aconitase 1; AKI: acute kidney injury; ARDS: acute respiratory distress syndrome; ATG: autophagy related; BECN1: beclin 1; CARM1/PRMT4: coactivator associated arginine methyltransferase 1; CIRBP: cold inducible RNA binding protein; CKD: chronic kidney disease; COPD: chronic obstructive pulmonary disease; ELAVL1: ELAV like RNA binding protein 1; Fer-1: ferrostatin-1; FTH1: ferritin heavy chain 1; GABARAP: GABA type A receptor-associated protein; GPX4: glutathione peroxidase 4; HAMP/hepcidin: hepcidin antimicrobial peptide; HCC: hepatocellular carcinoma; HERC2: HECT and RLD domain containing E3 ubiquitin protein ligase 2; HSCs: hepatic stellate cells; IL13: interleukin 13; IL6: interleukin 6; I/R: ischemia-reperfusion; IRE: iron-responsive element; IREB2/IRP2: iron responsive element binding protein 2; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MDA: malondialdehyde; MIOX: myo-inositol oxygenase; NCOA4: nuclear receptor coactivator 4; NFE2L2/Nrf2: NFE2 like bZIP transcription factor 2; ROS: reactive oxygen species; SIRT1: sirtuin 1; SLC40A1/ferroportin: solute carrier family 40 member 1; STAT3: signal transducer and activator of transcription 3; STEAP3: STEAP3 metalloreductase; TFRC/TfR1: transferrin receptor; USP11: ubiquitin specific peptidase 11; YAP1: Yes1 associated transcriptional regulator. - Source: PubMed
Publication date: 2026/02/23
Shao NingningYu HongzhiLi XueHan MinghuiChen ChengZhu JialinTang YuanyuanDong JinruiChen Huaiyong - Lung squamous cell carcinoma (LUSC) has a poor prognosis due to the lack of effective targeted therapies, and its incidence has increased dramatically in recent years, creating an urgent need for new prognostic markers. Given that tumor immune and metabolic heterogeneity can influence LUSC prognosis, this study aimed to construct a novel predictive model based on immune-related and metabolism-related genes for prognostic stratification in LUSC. Transcriptomic as well as clinical data of 502 and 43 LUSC cases were downloaded from The Cancer Genome Atlas Program (TCGA) and the Gene Expression Omnibus (GEO) databases. Core LUSC subtype genes were identified using nonnegative matrix factorization (NMF), and a prognostic risk model was subsequently constructed by applying machine learning, LASSO regression, and multivariate Cox regression. Based on this model, patients were stratified into low-risk and high-risk subgroups with distinct expression profiles and significant survival differences. Gene-Set Enrichment Analysis of the marker genes revealed that immune pathways were active in the high-risk group, whereas metabolic pathways were prominent in the low-risk group. The two groups also differed in tumor mutation burden and response to clinical therapy. High expression levels of NRTN, CYP2C18, TSLP, MIOX, and RORB and low expression levels of HBEGF, SERPIND1, PTGIS, and LBP were correlated with high survival rates. Immunohistochemical validation in 42 patients confirmed the expression patterns of the identified genetic markers, which were stronger in tumor tissues than in adjacent normal tissues. In conclusion, six immune-related and three metabolism-related genes were identified as prognostic markers of LUSC, with their expression levels significantly associated with the survival rate. The resulting model demonstrates strong predictive power and is expected to help guide treatment strategy decisions. - Source: PubMed
Xue HaoyuanLi HongweiHan SongyanZhang XiaqinLiu TongBu PengLiang Hua - Myo-inositol oxygenase (MIOX) plays an essential role in metabolic pathways and cell processes, controls oxidative stress response mechanisms, and balances osmotic stress in aquatic organisms. Molecular docking and structural analysis of the MIOX gene have been accomplished in this work. The MIOX gene has a length of 3608 bp, which encodes 286 amino acids (AA). The secondary structure revealed α-helical and random coils containing 40.56% alpha helices, 38.81% random coils, 14.69% extended strands, and 5.94% beta turns. The subcellular localization results showed that 56% of the MIOX gene is found in cytoplasm and then 10% in lysosome. The Ramachandran plot analysis showed that 90.2% of residues fall in the most favored region and 9.8% in the additional allowed region. Virtual screening of ligands and molecular docking of inositol (CID-892) and D-glucuronic acid (CID-94715) showed the highest docking score values of - 4.015 and - 3.563, respectively. The Potential Energy OPLS3e was - 1632.608 and - 1545.687. Inositol and D-glucuronic acid interacted with different residues of MIOX protein. However, a greater binding affinity of MIOX was observed with inositol than with D-glucuronic acid. This signifies the biochemical role of inositol that helps in determining the enzymatic efficiency. So, this study offers insights into protein modeling, molecular docking, and virtual screening of ligands against the MIOX receptor, revealing aspects of drug design and preventive approaches for fish salinity tolerance. - Source: PubMed
Publication date: 2026/01/05
Farooq SamraShafqat SamraKhan Jabbir AliWaheed AhmadUmar AliKhan Muhammad Saleem - The rising global CO level influences plant growth, productivity, and nutritional quality, and elevated CO (ECO) is commonly utilized in greenhouses to enhance vegetable crop yields. However, the molecular mechanism underlying plant responses to ECO remains unclear. This study examined the impacts of ECO on the nutritional quality and growth characteristics of two widely cultivated broccoli varieties, 'Yanxiu' and 'Qiuli'. A pot experiment was carried out in environmentally auto-controlled growth chambers over a period of 100 days, under both ambient CO (ACO, 420/470 ppm, daytime/nighttime) and ECO (700/750 ppm) conditions. Our results demonstrated that ECO significantly enhanced photosynthetic efficiency, increased head biomass accumulation, and elevated carbohydrate content. However, it also reduced free amino acids, soluble proteins, nitrate content, and mineral nutrients including nitrogen, potassium, calcium, iron, zinc, and copper, while increasing sulphur content in both varieties. Notably, ECO substantially increased health-promoting phytochemicals such as ascorbate, carotenoids, and total flavonoids. Through integrated transcriptomic and metabolomic analyses revealed: (1) ECO enhanced carbon metabolism via upregulation of hexokinase (HK), pyruvate kinase (PK), and Rubisco in glycolysis/pentose phosphate pathway; (2) activated biosynthesis of glucosinolates (via upregulating UDP-glucosyl transferase 83A, UGT83A, and cytochrome P450 81 F, CYP81F), flavonoids (via chalcone synthas, CHS, and flavonol synthase, FLS), ascorbate (via phospholipase C, PLC, and myo-inositol oxygenase, MIOX), and carotenoids (via phytotene synthase, PSY, and lycopene ε-cyclase, LCYE); and (3) suppressed nitrogen assimilation (via downregulating nitrate transporter 2, NRT2, and nitrate reductase, NR, and upregulating glutamine synthetase and glutamate synthase, GS/GOGAT). These findings systematically reveal that ECO reprograms broccoli metabolism to favor carbon assimilation while compromising nutrient acquisition. Our study provides valuable molecular insights for optimizing CO supplementation strategies in protected cultivation systems, offering potential solutions to balance yield improvement with nutritional quality maintenance in future vegetable production. - Source: PubMed
Publication date: 2025/12/07
Shi SongmeiLi HuakangGong YuefangWang XinjuHuang LiuYu PanpanXu JunqiangZheng'an YangHe Xinhua