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TXNRD1 encodes a member of the family of pyridine nucleotide oxidoreductases. Additionally we are shipping TXNRD1 Proteins (30) and TXNRD1 Kits (27) and many more products for this protein.
Showing 10 out of 115 products:
Human Polyclonal TXNRD1 Primary Antibody for ELISA, WB - ABIN184781
Gasdaska, Gasdaska, Cochran, Powis: Cloning and sequencing of a human thioredoxin reductase. in FEBS letters 1995
These data uncover a new role for NTRC in the control of photosynthetic yield.
An Arabidopsis thaliana double knockout mutant lacking NTRC and Srx (show SRX1 Antibodies) shows a phenotype similar to the ntrc mutant, while the srx (show SRX1 Antibodies) mutant resembles wild-type plants. NTRC deficiency causes reduced overoxidation of 2-Cys (show DNAJC5 Antibodies) 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 (show DNAJC5 Antibodies) peroxiredoxin with NADPH (show NQO1 Antibodies)-thioredoxin reductase C (NTRC) and thioredoxin (show TXN Antibodies) 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 (show NQO1 Antibodies)
analysis of electron transfer pathways and dynamics of chloroplast NADPH-dependent thioredoxin reductase C (NTRC)
NADPH (show NQO1 Antibodies)-thioredoxin reductase C (NTRC), previously reported as exclusive to green tissues, is also expressed in nonphotosynthetic tissues of Arabidopsis thaliana.
ANTR-C functions as an electron donor for plastidial 2-Cys (show DNAJC5 Antibodies) peroxiredoxins and represents the NADPH (show NQO1 Antibodies)-dependent thioredoxin/thioredoxin (show TXN Antibodies) reductase system in chloroplasts. [ANTR-C]
NTRC and 2-Cys (show DNAJC5 Antibodies) Prx (show PRX Antibodies) are involved in the protection of at least the later part of the chlorophyll biosynthetic pathway; NTRC and 2-Cys (show DNAJC5 Antibodies) Prx (show PRX Antibodies) in vitro stimulate the aerobic cyclase step of this pathway.
Selenoprotein TRXR-1 and GSR-1 (show GSR Antibodies) are essential for removal of old cuticle during molting in Caenorhabditis elegans.
Our findings demonstrate that elevated TrxR1 levels correlate with the acquisition of bortezomib resistance in MM. We propose considering TrxR1-inhibiting drugs, such as auranofin, either for single agent or combination therapy to circumvent bortezomib-resistance and improve survival outcomes of MM patients.
Cardamonin exposure and selenium availability regulate expression of HO-1 (show HMOX1 Antibodies), GPX2 (show GPX2 Antibodies) and TrxR1 in human intestinal cells.
Under the conditions of inhibition of TrxRs in cells, Parthenolide (PTL (show PNLIP Antibodies)) does not cause significant alteration of cellular thiol homeostasis, supporting selective target of TrxRs by PTL (show PNLIP Antibodies). Importantly, overexpression of functional TrxR1 or Trx1 (show MLL Antibodies) confers protection, whereas knockdown of the enzymes sensitizes cells to PTL (show PNLIP Antibodies) treatment.
TXNRD1_v1 and TXNRD1_v2 have distinct roles in differentiation, possibly by altering the expression of the genes associated with differentiation, and further emphasize the importance in distinguishing each unique action of different TrxR1 splice forms
Tissue microarrays containing human nevi and melanomas were used to evaluate levels of the antioxidant protein (show PRDX3 Antibodies) thioredoxin reductase 1 (TR1), which was found to increase as a function of disease progression.
Rheumatoid arthritis patients with high disease activity had significantly elevated TrxR levels in plasma and synovial fluid than did those with low disease activity.
TRX-1 (show MLL Antibodies)/PRX-1 (show PRDX1 Antibodies) levels are associated with NADPH oxidase (show NOX1 Antibodies)-activity in vivo and in vitro in atherosclerosis.
The association of TXNRD1 variability was found with physical performance, with three variants (rs4445711, rs1128446, and rs11111979) associated with physical functioning after 85 years of age.
In gene-based analysis of Se metabolism and selenoprotein candidate genes, only thioredoxin reductase 1 (TXNRD1) was significantly associated with toenail Selenium levels. [meta-analysis]
Expression of TrxR1 correlated highly with both the astrocytoma grade and proliferative index
The developmental expression of cytosolic glutathione peroxidase (show GPX1 Antibodies) 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 (show PRDX5 Antibodies) may act as a positive regulator of NF-kappa B (show NFKB1 Antibodies) and may play an important role in the cellular inflammatory response.
data provide evidence for the involvement of the Trx/TrxR (show GSR Antibodies) system, in the regulation of haem oxygenase-1 expression in aortic endothelial cells during pro-oxidant challenge
the timely upregulation of Trx1 (show TXN Antibodies)/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 (show SEP15 Antibodies) 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 (show SEPP1 Antibodies) has a thioredoxin (show TXN Antibodies) fold, Sepp1 (show SEPP1 Antibodies)(UF) were compared with full-length Sepp1 (show SEPP1 Antibodies), Sepp1 (show SEPP1 Antibodies)(Delta240-361), and Sepp1 (show SEPP1 Antibodies)(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.
The exaggerated TrxR release to serum upon liver injury may reflect more complex events than a mere passive release of hepatic enzymes to the extracellular milieu.
TrxR1-deficient cells are more sensitive to TNF-alpha (show TNF Antibodies) induced apoptosis than control cells.
Txnrd1-null livers did not have more effective gene expression responses to APAP challenge; however, their constitutive metabolic state supported more robust GSH biosynthesis, glutathionylation, and glucuronidation systems
TR1 protects against chemically induced hepatocarcinogenesis via the control of the cellular redox state, whereas its role in promoting this type of cancer is minimal
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