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the overexpression of thioredoxin,S100-A10 and S100-A6 specifically distinguished metastatic from non-metastatic tumors
Thioredoxin-h5 (TRXh5) reverses SNO modifications by acting as a selective protein-SNO reductase.
Data indicate that thioredoxin h proteins are not required to prevent the spontaneous activation of S-locus receptor kinase (SRK (show ZAP70 Proteins)) in the stigma.
Redox regulation of AtCPK21 by Trx-h1 in Arabidopsis thaliana in response to external stimuli is important for appropriate cellular responses.
in LOV1's absence, victorin inhibits TRX-h5, resulting in compromised defense but not disease by C. victoriae; in LOV1's presence, victorin binding to TRX-h5 activates LOV1 and elicits a resistance-like response that confers disease susceptibility
Structral model of thioredoxin h1 from Arabidopsis thaliana in the oxidized state displays the conserved thioredoxin fold.
Data show that thioredoxin h5 (ATTRX5), but not ATTRX3, is highly induced in sensitive Arabidopsis following victorin treatment.
regulation of NPR1 is through the opposing action of S-nitrosoglutathione and thioredoxins; findings suggest a link between pathogen-triggered redox changes and gene regulation in plant immunity
these findings demonstrate that Trx1 is a critical regulator of necroptosis that suppresses cell death by maintaining MLKL in a reduced inactive state.
Study shows that TRX1 (show MLL Proteins) and APEX1 (show APEX1 Proteins) expressions are up regulated in new Multiple Sclerosis (MS) patients compared to controls and might be implicated in pathogenesis of the disease.
CD40 (show CD40 Proteins) activation resulted in down-regulation of Thioredoxin (Trx)-1 to permit ASK1 (show MAP3K5 Proteins) activation and apoptosis. Although soluble receptor (show IFNAR1 Proteins) agonist alone could not induce death, combinatorial treatment incorporating soluble CD40 (show CD40 Proteins) agonist and pharmacological inhibition of Trx-1 (show MLL Proteins) was functionally equivalent to the signal triggered by mCD40L
our findings identify the TXN-FOXO1 (show FOXO1 Proteins)-p300 (show EP300 Proteins) circuit as the sensor and effector of oxidative stress in DLBCL cells
Novel positive feedback loop between Trx-1 (show MLL Proteins) and S100P (show S100P Proteins) promotes colorectal cancer invasion and metastasis.
Thioredoxin attenuates oxidized low-density lipoprotein induced oxidative stress in human umbilical vein endothelial cells by reducing NOX2 (show CYBB Proteins)-NOX4 (show NOX4 Proteins) activity.
from the two catalytic cysteines of TRX1 (show MLL Proteins) the residue C32 is responsible for the high-affinity binding of TRX1 (show MLL Proteins) to the ASK1 (show MAP3K5 Proteins)-TRX (show VAC14 Proteins)-binding domain in reducing conditions
findings suggest that the up-regulated RRM1 (show RRM1 Proteins) and hTrx1 (show MLL Proteins) in colorectal cancer directly interact with each other and promote RR activity, resulting in enhanced DNA synthesis and cancer malignancy.
findings support the potential pathophysiological relevance of TRX (show VAC14 Proteins) in celiac disease and establish the Cys (show DNAJC5 Proteins)(370)-Cys (show DNAJC5 Proteins)(371) disulfide bond of TG2 (show TGM2 Proteins) as one of clearest examples of an allosteric disulfide bond in mammals.
Trx (show VAC14 Proteins) and its target proteins involved in redox signaling are critical for the control of cell fate such as cell survival and apoptosis [review]
single-marker and haplotype analyses revealed significant effects of TXNIP (show TXNIP Proteins) on hot carcass weight, test daily gain, and lifetime daily gain
Trx1 enhances blood perfusion and increases angiogenic protein expression in a rodent hind limb ischemia model.
GSR (show GSR Proteins) is not essential for the maintenance of antioxidant defenses in mouse cochlea; the thioredoxin/thioredoxin reductase (show PRDX2 Proteins) system can probably operate as a functional backup for GSR (show GSR Proteins).
These results strongly suggest that Trx1 ameliorates the myocardial effects of I/R by improving the free radical-mediated damage in cardiac and mitochondrial function, opening the possibility of new therapeutic strategies in coronary artery disease.
findings support the potential pathophysiological relevance of TRX in celiac disease and establish the Cys (show DNAJC5 Proteins)(370)-Cys (show DNAJC5 Proteins)(371) disulfide bond of TG2 (show TGM2 Proteins) as one of clearest examples of an allosteric disulfide bond in mammals.
Thioredoxin-mediated deglutathionylation of eNOS (show NOS3 Proteins) in the coronary artery in vivo protected against reperfusion injury, even in the presence of normal levels of glutathione.
Acute stimuli of epinephrine induced Trx-1 expression through activating CREB (show CREB1 Proteins).
results suggest that PostC prevents Trx-1 degradation, decreasing oxidative stress and allowing the activation of Akt and GSK3beta to exert its cardioprotective effect
blocking MPTP (show PTPN2 Proteins)-mediated TNF (show TNF Proteins) signaling through intrathecal administration of TNF (show TNF Proteins)-neutralizing antibody prevented Trx1 oxidation and downstream ASK1 (show MAP3K5 Proteins)-p38 MAPK (show MAPK14 Proteins) activation
GL-V9 attenuated DSS (show PMP22 Proteins)-induced colitis against oxidative stress by up-regulating Trx-1 via activation of AMPK (show PRKAA1 Proteins)/FOXO3a (show FOXO3 Proteins) pathway.
The ventral signal observed from E12.5 onward colocalized with motor neuron markers Isl1 (show ISL1 Proteins)/2 and FoxP1 (show FOXP1 Proteins). and the strong ventral signal colocalizing with Isl1 (show ISL1 Proteins)/2 was observed in all rostrocaudal segments of the spinal cord
The protein encoded by this gene acts as a homodimer and is involved in many redox reactions. The encoded protein is active in the reversible S-nitrosylation of cysteines in certain proteins, which is part of the response to intracellular nitric oxide. This protein is found in the cytoplasm. Two transcript variants encoding different isoforms have been found for this gene.
, thioredoxin-like protein
, peptidase C
, ATL-derived factor
, TXN delta 3
, surface-associated sulphydryl protein
, thioredoxin delta 3