Ask about this productRelated genes to: FDXR Blocking Peptide
- Gene:
- FDXR NIH gene
- Name:
- ferredoxin reductase
- Previous symbol:
- ADXR
- Synonyms:
- ADR
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-06-09
- Date modifiied:
- 2019-03-12
Related products to: FDXR Blocking Peptide
Related articles to: FDXR Blocking Peptide
- - Source: PubMed
Publication date: 2026/04/28
Hong HanqingSun JunyanWeng LichunHou LinXiao ChengqiWang QianLai Dongmei - Ionizing radiation is a potent genotoxic carcinogen. In this study, acute DNA damage-related biomarker responses were evaluated in peripheral blood lymphocytes of adults undergoing radiographic investigations for orthodontic treatment. Patients (n = 22) for orthodontic treatment were divided into two groups: Group 1 - conventional radiographs (Orthopantomogram (OPG), Lateral Cephalogram (LC) and two Intra-oral periapical radiographs); Group 2 - Cone Beam Computed Tomography (CBCT). Peripheral blood samples (3 mL) were collected before and after radiography imaging. Gamma-H2AX (γ-H2AX) focus formation, micronucleus (MN) formation, and ferredoxin reductase (FDXR) gene expression were evaluated as biomarkers of exposure and response. The frequency of γ-H2AX focus and micronuclei increased significantly (p < 0.05 and p < 0.001) from pre- and post-radiography in both groups. FDXR showed significant upregulation and downregulation in Groups 1 and 2, respectively indicating divergent early transcriptional response between the groups. Conventional radiographs and low-dose CBCT exerted acute DNA damage-related biomarker responses in adult orthodontic patients. FDXR gene showed greater upregulation with conventional radiographs than CBCT. Group 1 and group 2 post-radiography showed no statistical difference when assessed with the three biomarkers for acute damage. Future studies with larger samples and long-term follow-up are needed to validate the findings and provide a basis for safety recommendations. - Source: PubMed
Publication date: 2026/02/28
Murali SandhyaKannan NandhiniKailasam VigneshPerumal VenkatachalamMandodi Mohammed - B cells are crucial for adaptive immunity, orchestrating humoral responses by producing antibodies essential for pathogen clearance. Here, we show that Poly(rC) binding protein 1 (), a multifunctional RNA binding protein, is a key regulator of antibody production in B cells. deficiency in B cells resulted in significant reductions in immunoglobulin M expression at steady state and compromised differentiation of germinal center B cells and production of high-affinity antibodies upon immunization. These effects were caused by defective mitochondrial integrity in -deficient B cells, including impaired mitochondrial electron transport chain complex I and elevated mitochondrial reactive oxygen species production. Mechanistically, binds to the 3' untranslated region of messenger RNA to promote its expression, thereby supporting iron-sulfur cluster biogenesis, the assembly of mitochondrial complex I, and other Fdxr-dependent processes. Our findings reveal a previously unidentified role for in regulating mitochondrial function, protein synthesis, and antibody responses in B cells, providing insight into posttranscriptional regulation and mitochondrial functions in adaptive immunity. - Source: PubMed
Publication date: 2026/04/10
Zhu LizhenLin LiQi TuanLi GengLiang ZhixingYu JianchengFu YifanPeng YueChang Xing - Ferredoxin reductase (FDXR) is the sole ferredoxin reductase in humans and plays an essential role for steroidogenesis and biosynthesis of heme and iron-sulfur cluster (ISC) by transferring electrons from NADPH to ISC-containing ferredoxin 1 (FDX1) and FDX2. In this study, we found that while FDXR is classified as a mitochondria-localized flavoprotein, it can be translocated into the nucleus, especially in response to various stress signals. Next, we identified a bipartite nuclear localization signal within amino acids 271-299 of FDXR, the disruption of which impairs its nuclear translocation. Further, we found that AKT can phosphorylate threonine 277 adjacent to the NLS in FDXR and subsequently enhances its nuclear translocation. Consistent with this, mutant FDXR(T277A), in which threonine 277 was substituted with alanine, impaired FDXR nuclear translocation. Together, our data provide evidence that the mitochondrial FDXR can be translocated to the nucleus, which is regulated by AKT-mediated phosphorylation, especially in response to cellular stress. Our data suggest that FDXR plays a role in the mitochondria-nucleus communication and stress responses. - Source: PubMed
Nakajima Ken-IchiMohibi ShakurChen XinbinZhang Jin - -related disorders (FRDs) are rare mitochondrial conditions typically presenting with progressive optic atrophy and neuropathy. We report identical twins presenting with acute-onset flaccid quadriparesis following a respiratory infection, expanding the known phenotypic spectrum of variants. - Source: PubMed
Publication date: 2026/02/23
Tafakhori AbbasSarvestani ZahraKariminejad ArianaTajsharghi HomaSeo Go HunRyu Seung WooHeydari Havadaragh Sanaz