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Human TXNRD1 ELISA Kit für Sandwich ELISA - ABIN2685846
Mustacich, Powis: Thioredoxin reductase. in The Biochemical journal 2000
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NTRC-mediated regulation of the Calvin-Benson cycle and ATP synthesis occurs both directly and through interaction with the ferredoxin-thioredoxin (zeige TXN ELISA Kits) system and is crucial when availability of light is limiting photosynthesis.
NTRC is highly sensitive to rapidly changing light intensities.NTRC is not responsible for 'metabolism-related' regulation of the ATP synthase.
cooperative control of chloroplast functions via the FTR/Trx (zeige TXN ELISA Kits) and NTRC pathways is essential for plant viability
These data uncover a new role for NTRC in the control of photosynthetic yield.
An Arabidopsis thaliana double knockout mutant lacking NTRC and Srx (zeige SRX1 ELISA Kits) shows a phenotype similar to the ntrc mutant, while the srx (zeige SRX1 ELISA Kits) mutant resembles wild-type plants. NTRC deficiency causes reduced overoxidation of 2-Cys (zeige DNAJC5 ELISA Kits) peroxiredoxins.
NADPH thioredoxin reductase C is involved in redox regulation of the Mg-chelatase I subunit in Arabidopsis thaliana chloroplasts
interaction of chloroplast 2-Cys (zeige DNAJC5 ELISA Kits) peroxiredoxin with NADPH (zeige NQO1 ELISA Kits)-thioredoxin reductase C (NTRC) and thioredoxin (zeige TXN ELISA Kits) x
The strongest reduction in ntrc growth occurred under photoperiods with nights longer than 14 h, whereas knockout of the NTRC gene did not alter the circadian-clock-controlled growth. Lack of NTRC modulated chloroplast reactive oxygen species metabolism.
heat shock-mediated holdase chaperone function of NTRC is responsible for the increased thermotolerance of Arabidopsis and the activity is significantly supported by NADPH
analysis of electron transfer pathways and dynamics of chloroplast NADPH-dependent thioredoxin reductase C (NTRC)
Selenoprotein TRXR-1 and GSR-1 (zeige GSR ELISA Kits) are essential for removal of old cuticle during molting in Caenorhabditis elegans.
Endogenous TrxR1 is sensitive to nitrosylation-dependent inactivation.
This study thus provides novel insights into the catalytic mechanisms of TrxR1. One-electron juglone reduction by TrxR1 producing superoxide should furthermore contribute to the well-known prooxidant cytotoxicity of juglone
Mutation of TXNRD1 was identified in a family with genetic generalized epilepsy.
Data show that small molecule B19 targets and inactivates thioredoxin reductase 1 (TrxR1) in gastric cancer cells.
Analysis of 25 independent cohorts with 5910 patients showed that Trx1 (zeige MLL ELISA Kits) and TrxR1 were both associated with a poor patient prognosis in terms of overall survival, distant metastasis free survival and disease free survival.
High TRXR1 expression is associated with oral squamous cell carcinoma.
Inhibition of thioredoxin reductase-1 by brevetoxin-2 is via the formation of a Michael adduct between selenocysteine and the alpha, beta-unsaturated aldehyde moiety of the toxin.
Here, the authors use a novel assay to demonstrate that the reduction in non-native disulfides requires NADPH (zeige NQO1 ELISA Kits) as the ultimate electron donor, and a robust cytosolic thioredoxin (zeige TXN ELISA Kits) system, driven by thioredoxin reductase 1 (TrxR1 or TXNRD1).
Taken together, these findings indicate that auranofin inhibition of TrxR activity in Hep3B cells activates ROS (zeige ROS1 ELISA Kits)- and caspase (zeige CASP3 ELISA Kits)-dependent apoptotic signaling pathways and triggers cancer cell death.
It was observed that the combination of redox/protonation states of the N-terminal (FAD (zeige BRCA2 ELISA Kits) and Cys59/64) and C-terminal (Cys497/Selenocysteine498) redox centers defines the preferred relative positions and allows for the flexible arm to work as the desired electron "shuttle."
The developmental expression of cytosolic glutathione peroxidase (zeige GPX1 ELISA Kits) and TRXR1 during fetal development and the effect of maternal selenium consumption on the expression of these proteins are reported.
regenerated coronary endothelial cells exhibit downregulation of thioredoxin reductase
These results suggest that thioredoxin reductase (zeige PRDX5 ELISA Kits) may act as a positive regulator of NF-kappa B (zeige NFKB1 ELISA Kits) and may play an important role in the cellular inflammatory response.
data provide evidence for the involvement of the Trx/TrxR (zeige GSR ELISA Kits) system, in the regulation of haem oxygenase-1 expression in aortic endothelial cells during pro-oxidant challenge
GSR (zeige GSR ELISA Kits) is not essential for the maintenance of antioxidant defenses in mouse cochlea; the thioredoxin/thioredoxin (zeige TXN ELISA Kits) reductase (zeige PRDX2 ELISA Kits) system can probably operate as a functional backup for GSR (zeige GSR ELISA Kits).
TrxR1 represents a novel therapeutic target to prevent oxygen-mediated neonatal lung injury through Nrf2 (zeige NFE2L2 ELISA Kits).
The results demonstrate that DATS protects against oxidative stress-induced (zeige SQSTM1 ELISA Kits) DNA damage and apoptosis in C2C12 cells in part through the activation of Nrf2 (zeige NFE2L2 ELISA Kits)-mediated TrxR1 induction via the ERK (zeige EPHB2 ELISA Kits) signaling pathway.
Collectively, our results suggest that MsrA (zeige MSR1 ELISA Kits) protects hepatocytes from APAP-induced cytotoxicity through the modulation of TXNRD1 expression.
the timely upregulation of Trx1 (zeige TXN ELISA Kits)/TrxR1 and the active control of intracellular redox status is critical for the survival of thymocytes during and short after positive selection.
Considering the variable expression levels of Sep15 and TR1 found within the human population, our results provide insights into new roles of selenoproteins in cancer
Data suggest TXNRD1 and TXRNRD2 function at the top of a redox pyramid that governs the oxidation state of peroxiredoxins and other protein factors, thereby dictating a hierarchy of phenotypic responses to oxidative insults.
Augmentation of GSH systems by TrxR1 inhibition could represent a promising therapeutic approach to attenuate oxidant-mediated lung injury and improve patient outcomes.
Because the N-terminal domain of Sepp1 (zeige SEPP1 ELISA Kits) has a thioredoxin (zeige TXN ELISA Kits) fold, Sepp1 (zeige SEPP1 ELISA Kits)(UF) were compared with full-length Sepp1 (zeige SEPP1 ELISA Kits), Sepp1 (zeige SEPP1 ELISA Kits)(Delta240-361), and Sepp1 (zeige SEPP1 ELISA Kits)(U40S) as a substrate of thioredoxin reductase-1 (TrxR1).
Sec-containing TrxR1 is absolutely required for self-sufficient growth of MEFs under high-glucose conditions, owing to an essential importance of this enzyme for elimination of glucose-derived H2O2.
This gene encodes a member of the family of pyridine nucleotide oxidoreductases. This protein reduces thioredoxins as well as other substrates, and plays a role in selenium metabolism and protection against oxidative stress. The functional enzyme is thought to be a homodimer which uses FAD as a cofactor. Each subunit contains a selenocysteine (Sec) residue which is required for catalytic activity. The selenocysteine is encoded by the UGA codon that normally signals translation termination. The 3' UTR of selenocysteine-containing genes have a common stem-loop structure, the sec insertion sequence (SECIS), that is necessary for the recognition of UGA as a Sec codon rather than as a stop signal. Alternative splicing results in several transcript variants encoding the same or different isoforms.
thioredoxin reductase 1, cytoplasmic
, thioredoxin reductase 3
, thioredoxin reductase 1
, thioredoxin reductase 1, cytoplasmic-like
, KM-102-derived reductase-like factor
, gene associated with retinoic and IFN-induced mortality 12 protein
, gene associated with retinoic and interferon-induced mortality 12 protein
, thioredoxin reductase GRIM-12
, thioredoxin reductase TR1
, redox enzyme thioredoxin reductase
, NADPH-dependent thioredoxin reductase
, selenoprotein oxidoreductase
, TR alpha