NDOR1

Last update 08 May 2025

Basic Info

Synonyms

bA350O14.9, CIAE1, NADPH dependent diflavin oxidoreductase 1

+ [5]

Introduction

NADPH-dependent reductase which is a central component of the cytosolic iron-sulfur (Fe-S) protein assembly (CIA) machinery (PubMed:10625700, PubMed:15900210, PubMed:20802492, PubMed:23596212, PubMed:28648056). Transfers electrons from NADPH via its FAD and FMN prosthetic groups to the [2Fe-2S] cluster of CIAPIN1, another key component of the CIA machinery (PubMed:20802492, PubMed:23596212, PubMed:28648056). In turn, this reduced cluster provides electrons for assembly of cytosolic iron-sulfur cluster proteins (PubMed:20802492, PubMed:23596212). It can also reduce the [2Fe-2S] cluster of CISD1 and activate this protein implicated in Fe/S cluster repair (PubMed:28648056). In vitro can fully activate methionine synthase/MTR in the presence of soluble cytochrome b5/CYB5A (PubMed:12871938).

100 Clinical Results associated with NDOR1

100 Translational Medicine associated with NDOR1

0 Patents (Medical) associated with NDOR1

2,986

Literatures (Medical) associated with NDOR1

01 Mar 2025·Plant Science

Differential regulation of the “phytoglobin-nitric oxide respiration” in Medicago truncatula roots and nodules submitted to flooding

Article

Author: Berger, Antoine ; Boscari, Alexandre ; Mhadhbi, Haythem ; Chammakhi, Chaïma ; Pacoud, Marie ; Brouquisse, Renaud ; Gharbi, Imène

Flooding induces hypoxia in plant tissues, impacting various physiological and biochemical processes. This study investigates the adaptive response of the roots and nitrogen-fixing nodules of Medicago truncatula in symbiosis with Sinorhizobium meliloti under short-term hypoxia caused by flooding. Four-week-old plants were subjected to flooding for 1-4 days. Physiological parameters as well as the expression of the senescence marker gene MtCP6 remained unchanged after 4 days of flooding, indicating no senescence onset. Hypoxia was evident from the first day, as indicated by the upregulation of hypoxia marker genes (MtADH, MtPDC, MtAlaAT, MtERF73). Nitrogen-fixing capacity was unaffected after 1 day but markedly decreased after 4 days, while energy state (ATP/ADP ratio) significantly decreased from 1 day and was more affected in nodules than in roots. Nitric oxide (NO) production increased in roots but decreased in nodules after prolonged flooding. Nitrate reductase (NR) activity and expression of genes associated with Phytoglobin-NO (Pgb-NO) respiration (MtNR1, MtNR2, MtPgb1.1) were upregulated, suggesting a role in maintaining energy metabolism under hypoxia, but the use of M. truncatula nr1 and nr2 mutants, impaired in nitrite production, indicated the involvement of these two genes in ATP regeneration during initial flooding response. The addition of sodium nitroprusside or tungstate revealed that Pgb-NO respiration contributes significantly to ATP regeneration in both roots and nodules under flooding. Altogether, these results highlight the importance of NR1 and Pgb1.1 in the hypoxic response of legume root systems and show that nodules are more sensitive than roots to hypoxia.

01 Mar 2025·Behavioural Brain Research

Molecular and behavioral effects of Acamprosate in male rats with sodium salicylate-induced tinnitus

Article

Author: Shahbazi, Ali ; Mahmoudian, Saeid ; Akbarnejad, Zeinab ; Farhadi, Mohammad ; Farrahizadeh, Maryam ; Joghataei, Mohammad Taghi

BACKGROUNDImbalance in inhibitory and excitatory neurotransmitters have been reported in tinnitus. Acamprosate modulates the excitatory and inhibitory neurotransmission in the nucleus accumbens (NAc). This study aims to assess the effect of Acamprosate on tinnitus, anxiety, depression, and molecular changes in nucleus accumbens (NAc), in Sodium-Salisylate (S-salicylate) model of tinnitus.METHODSForty-four adult male wistar rats were used in this study. The study included Control, Saline, and S-salicylate groups during the first week, which then subdivided into five groups as Control, Saline, S-salicylate, Acamprosate, and S-salicylate+Acamprosate. Gap-in Noise (GIN) and pre-pulse inhibition (PPI) were used to assessment of tinnitus at baseline, day7 and day14. Anxiety and depression were evaluated on day 14, by elevated plus maze (EPM), open field (OF), and tail suspension (TST) tests. The protein expression of GABAAR-δ, NR1 and NR2B in NAc were also measured using western blot technique.RESULTSAfter seven days GIN reduced in S-salicylate compare to Control and Saline groups (P < 0.5), while PPI unchanged. After 14 days, GIN reduced in S-salicylate and S-salicylate+Acamprosate groups compare to Control; Saline; and Acamprosate groups (P < 0.5). Additionally, GIN was higher in S-salicylate+Acamprosate compare to S-salicylate group (P < 0.5). PPI was not changed after 14 days. Open arm time in EPM test was decreased in S-salicylate and S-salicylate+Acamprosate groups compare to Control; Saline; and Acamprosate groups (P < 0.5). Central Zone time in OF test was reduced in S-salicylate group compare to Control, Saline, Acamprosate, and S-salicylate+Acamprosate groups (P < 0.5). Immobility Time in TST was increased in S-salicylate group compare to Control, Saline, Acamprosate, and S-salicylate+Acamprosate groups (P < 0.5). GABAAR-δ was decreased in S-salicylate groups compare to Control, Saline, Acamprosate; and S-salicylate+Acamprosate groups (P < 0.5). NR1 and NR2B in NAc were increased in S-salicylate group compare to Control, Saline, Acamprosate, and S-salicylate+Acamprosate groups (P < 0.5).CONCLUSIONS-salicylate can induce tinnitus-like behaviors in rat. Furthermore, S-salicylate induced depression/anxiety like behaviors, and changed the expression of GABAR and NMDAR subunits in NAc. Acamprosate partially reversed these changes. In conclusion, NAc may be involved in the pathophysiologic mechanisms of tinnitus.

01 Mar 2025·Phytomedicine

Notoginsenoside R1 alleviates blue light-induced corneal injury and wound healing delay by binding to and inhibiting TRIB1

Article

Author: Tong, Jianping ; Wang, Xinglin ; Li, Yuanyuan ; Chen, Kuangqi ; Shen, Chang ; Wang, Yinhao ; Li, Xiang ; Xia, Yutong ; Li, Xiuyi ; Chen, Zhitong ; Song, Dongjie ; Yu, Xin ; Li, Jiafeng ; Shen, Ye

BACKGROUNDWith the escalating use of digital devices, blue light (BL) exposure has emerged as a critical concern due to its potential to cause ocular damage. This study explores the protective effects of notoginsenoside R1 (NR1), a bioactive compound from Panax notoginseng (Burkill) F.H. Chen (Sanqi), against BL-induced corneal epithelial injury.PURPOSEThis research aims to investigate the protective effects of NR1 on BL-induced corneal injury and wound healing delay.METHODSHuman corneal epithelial cells (hCECs) were pretreated with NR1 (0-50 μM) or N-acetylcysteine (NAC, 10 mM), then exposed to BL (570 μW/cm²) for 24 h. Cell viability, proliferation, migration, and ROS levels were assessed using various techniques. In mice, NR1 (25 μM and 50 μM) and NAC (0.3 %) eye drops were administered during BL exposure. Corneal injury, healing rates, cell proliferation, migration, ROS, and inflammation were evaluated. RNA-sequencing, bioinformatics, and molecular binding validation identified tribbles homolog 1 (TRIB1) as a key molecule mitigating BL damage with NR1. Functional studies via gene silencing, overexpression, and pharmacological modulation further explored TRIB1's role in BL exposure.RESULTSNR1 significantly reduced BL-induced inflammation, ROS production, and inhibited migration and proliferation in hCECs and murine corneas. It also alleviated BL-induced corneal injury and delayed healing in mice. NR1 inhibited TRIB1 upregulation, a marker of BL-induced injury and healing delay. Overexpression of TRIB1 negated NR1's therapeutic effects on hCECs, while TRIB1 silencing mitigated functional impairment. In mice, increased Trib1 expression caused corneal injury and delayed healing, reversed by NR1 treatment.CONCLUSIONNR1 shows potential as a therapeutic agent by inhibiting TRIB1 elevation in response to BL exposure, providing a novel promising target for corneal injury and wound healing delay induced by BL, and offering a comprehensive strategy for clinical pharmacological intervention.

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