Ask about this productRelated genes to: OXR1 antibody
- Gene:
- OXR1 NIH gene
- Name:
- oxidation resistance 1
- Previous symbol:
- -
- Synonyms:
- TLDC3
- Chromosome:
- 8q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-14
- Date modifiied:
- 2016-10-05
Related products to: OXR1 antibody
Related articles to: OXR1 antibody
- Amyotrophic lateral sclerosis (ALS) lacks reliable and minimally invasive biomarkers for early diagnosis. m6A-associated single-nucleotide polymorphisms (m6A-SNPs) may influence RNA methylation and gene expression, offering opportunities to identify clinically relevant diagnostic markers. - Source: PubMed
Publication date: 2026/08/27
Wang HongfenSun BoWang ShiyaPan JingDu RongrongPang XinyuanBai JiongmingHan JinmingFeng Jinli - Many age-related neurodegenerative disorders are marked by progressive defects in cellular energy metabolism and protein homeostasis that converge on mitochondrial and lysosomal dysfunction. TLDc domain-containing proteins, such as OXR1, NCOA7, and related family members, have emerged as crucial modulators of organellar physiology and cellular stress responses. Growing evidence indicates that TLDc proteins physically interact with vacuolar ATPases (V-ATPases) to modulate their assembly and catalytic activity, linking TLDc function directly to the maintenance of lysosomal and Golgi lumen pH. This organellar pH homeostasis, in turn, is fundamental to intracellular iron handling and metabolic regulation, processes essential for mitochondrial bioenergetics, lysosomal functions, and cellular viability. Lysosomes maintain an acidic lumen via V-ATPase proton pumping, counterbalanced by specific ion channels, including TMEM175. This acidic environment is required for ferric iron reduction and subsequent release into the cytosol; when acidification fails, cells develop cytosolic iron deficiency, mitochondrial defects, pseudohypoxia via HIF-1α activation, and inflammation. Conversely, iron flux from lysosomes to mitochondria depends on acidic conditions and direct organelle contact, as exemplified by BDH2-driven siderophore transport, a V-ATPase-dependent but not TLDc-regulated process, which supports mitochondrial bioenergetics and sustains lysosomal acidity. Iron and pH dysregulation synergize to drive ferroptosis, lipid peroxidation, and neurotoxicity. Emerging studies link lysosomal deacidification and iron dyshomeostasis to the pathogenesis of major neurodegenerative diseases. These mechanisms collectively shape neuronal resilience, survival, and aging trajectories. This review integrates recent insights into how TLDc proteins coordinate organellar pH regulation and iron homeostasis and discusses how disruption of these interconnected pathways contributes to age-related neurodegeneration. - Source: PubMed
Publication date: 2026/09/01
Ghufran Mohammad SajidSoni PriyankaThomas Bobby - In Parkinson's disease and other synucleinopathies, αSynuclein (αSyn) misfolds and forms Ser-phosphorylated aggregates (pSyn) with the factors controlling this process largely unknown. Here, we used arrayed CRISPR-mediated gene activation and ablation to discover new pSyn modulators. Using quadruple-guide RNAs (qgRNAs) and Cas9, or an inactive Cas9 fused to a synthetic transactivator, we ablated 2304 and activated 2428 human genes related to mitochondria, trafficking, and motility functions in HEK293 cells. After exposure of cells to αSyn fibrils, pSyn signals were recorded by high-throughput fluorescence microscopy and aggregates were identified by image analysis. We found that pSyn was increased by activating the mitochondrial protein OXR1, which decreased ATP levels and altered the mitochondrial membrane potential. Instead, pSyn was reduced by ablation of the endoplasmic reticulum (ER)-associated protein EMC4, which enhanced ER-driven autophagic flux and lysosomal clearance. OXR1 activation preferentially modulated cellular reactions to fibrils derived from multiple system atrophy (MSA) patients, whereas EMC4 ablation broadly reduced pSyn across diverse αSyn polymorphs. These findings were confirmed in human iPSC-derived cortical and dopaminergic neurons, where OXR1 preferentially promoted somatic aggregation and EMC4 reduced both somatic and neuritic aggregates. These results uncover previously unrecognized roles for OXR1 and EMC4 in αSyn aggregation, thereby broadening our mechanistic understanding of synucleinopathies. - Source: PubMed
Publication date: 2026/03/30
Neupane SandeshNikolić LeaMaraio LorenzoGoiran ThomasKarpilovsky NathanSellitto StefanoBouris VangelisYin Jiang-AnMelki RonaldFon Edward AAguzzi AdrianoDe Cecco Elena - Methadone maintenance treatment (MMT) is one of the major pharmacotherapies for opioid use disorder. The underlying mechanisms of addiction and the treatment response are only partially understood. The study's main goal was to identify differential DNA CpG methylation that occurred in response to MMT. - Source: PubMed
Publication date: 2026/03/05
Levran OrnaKim YuliLi JustinSason AnatAdelson MiriamPeles Einat - This study aimed to investigate the effects of the "living high-training low" (LHTL) model, in which mice were housed under hypoxic conditions but trained in normoxia to maintain training quality. We analyzed key proteins involved in cellular metabolism and oxidative stress, including hypoxia-inducible factor 1α (HIF-1α), peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), and oxidation resistance protein 1 (OXR1). Forty male isogenic C57BL/6J mice were divided into nontrained (N) and trained (T) groups living in normoxic (NOR) or hypoxic (HYP) environments. HYP mice were housed 18 h/day for 8 weeks in a normobaric tent supplied with oxygen-depleted air (FiO = 14.5%). Animal handling, including training, was conducted in normoxia (FiO = 19.5%). Training occurred 5 times/week (40 min/session) at ~80% of individual critical velocity. All mice were euthanized to extract the soleus, white gastrocnemius, and hypothalamus for protein analysis. Compared with training alone, LHTL did not lead to significantly greater HIF-1α, PGC-1α, or OXR1 expression across tissues; however, induced behavioral changes-such as reduced spontaneous physical activity and diminished ability to complete training-may indicate that the demands of the LHTL model were not trivial. - Source: PubMed
Scariot Pedro P MPapoti MarceloPolisel Emanuel E COrsi Juan BHill David WManchado-Gobatto Fúlvia BGobatto Claudio A