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Human Monoclonal TXN Primary Antibody pour ICS, WB - ABIN967658
Bertini, Howard, Dong, Oppenheim, Bizzarri, Sergi, Caselli, Pagliei, Romines, Wilshire, Mengozzi, Nakamura, Yodoi, Pekkari, Gurunath, Holmgren, Herzenberg, Herzenberg, Ghezzi: Thioredoxin, a redox enzyme released in infection and inflammation, is a unique chemoattractant for neutrophils, monocytes, and T cells. dans The Journal of experimental medicine 1999
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Human Polyclonal TXN Primary Antibody pour IF (p), IHC (p) - ABIN668871
Li, Sun, Xiao, Sun: First characterization of a teleost Epstein-Barr virus-induced gene 3 (EBI3) reveals a regulatory effect of EBI3 on the innate immune response of peripheral blood leukocytes. dans Developmental and comparative immunology 2013
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Human Monoclonal TXN Primary Antibody pour IHC (fro), IHC (p) - ABIN2476763
Poole, Morgan, Bebbington: Analysis of ecdysones by gas chromatography using electron capture detection. dans Journal of chromatography 1975
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Human Monoclonal TXN Primary Antibody pour IHC (fro), IHC (p) - ABIN151171
Perkins, Di Trapani, McKay, Clarke: Immunocytochemical localization of thioredoxin in human trophoblast and decidua. dans Placenta 1996
Human Monoclonal TXN Primary Antibody pour IF, IP - ABIN563300
Ahrens, Timme, Ostendorp, Bogatyreva, Hoeppner, Hopt, Hauschke, Werner, Lassmann: Response of esophageal cancer cells to epigenetic inhibitors is mediated via altered thioredoxin activity. dans Laboratory investigation; a journal of technical methods and pathology 2016
Increased serum thioredoxin concentrations are highly associated with trauma severity
Plasma-TRX on day 1 was significantly increased in patients who later developed (Montrer VAC14 Anticorps) post-injury sepsis. In a logistic regression analysis including TRX, C-reactive protein, injury severity, massive transfusion, and admission blood pressure, TRX was the only variable independently associated with post-injury sepsis
High TRX1 (Montrer MLL Anticorps) expression is associated with myocardial infarction.
Data show that suberoylanilide hydroxamic acid (SAHA) induced apoptosis via the down-regulation thioredoxin1 (Trx1 (Montrer MLL Anticorps)), which was regulated by microRNA miR (Montrer MLXIP Anticorps)-129-5p.
Analysis of 25 independent cohorts with 5910 patients showed that Trx1 (Montrer MLL Anticorps) and TrxR1 (Montrer TXNRD1 Anticorps) were both associated with a poor patient prognosis in terms of overall survival, distant metastasis free survival and disease free survival.
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 (Montrer MLL Anticorps) and APEX1 (Montrer APEX1 Anticorps) expressions are up regulated in new Multiple Sclerosis (MS) patients compared to controls and might be implicated in pathogenesis of the disease.
CD40 (Montrer CD40 Anticorps) activation resulted in down-regulation of Thioredoxin (Trx)-1 to permit ASK1 (Montrer MAP3K5 Anticorps) activation and apoptosis. Although soluble receptor (Montrer IFNAR1 Anticorps) agonist alone could not induce death, combinatorial treatment incorporating soluble CD40 (Montrer CD40 Anticorps) agonist and pharmacological inhibition of Trx-1 (Montrer MLL Anticorps) was functionally equivalent to the signal triggered by mCD40L
our findings identify the TXN-FOXO1 (Montrer FOXO1 Anticorps)-p300 (Montrer EP300 Anticorps) circuit as the sensor and effector of oxidative stress in DLBCL cells
Novel positive feedback loop between Trx-1 (Montrer MLL Anticorps) and S100P (Montrer S100P Anticorps) promotes colorectal cancer invasion and metastasis.
A novel mouse model for the identification of thioredoxin-1 protein interactions has been created.
Serum thioredoxin reductase (Montrer PRDX2 Anticorps) is highly increased in mice with hepatocellular carcinoma and its activity is restrained by several mechanisms, in particular, by the serum QSOX1 (Montrer QSOX1 Anticorps).
Nuclear overexpression of Trx1 restored Nrf2 (Montrer NFE2L2 Anticorps) activity and attenuated alcohol-induced acute lung injury.
Trx1 enhances blood perfusion and increases angiogenic protein expression in a rodent hind limb ischemia model.
GSR (Montrer GSR Anticorps) is not essential for the maintenance of antioxidant defenses in mouse cochlea; the thioredoxin/thioredoxin reductase (Montrer PRDX2 Anticorps) system can probably operate as a functional backup for GSR (Montrer GSR Anticorps).
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 (Montrer DNAJC5 Anticorps)(370)-Cys (Montrer DNAJC5 Anticorps)(371) disulfide bond of TG2 (Montrer TGM2 Anticorps) as one of clearest examples of an allosteric disulfide bond in mammals.
Thioredoxin-mediated deglutathionylation of eNOS (Montrer NOS3 Anticorps) 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 (Montrer CREB1 Anticorps).
results suggest that PostC prevents Trx-1 degradation, decreasing oxidative stress and allowing the activation of Akt (Montrer AKT1 Anticorps) and GSK3beta (Montrer GSK3b Anticorps) to exert its cardioprotective effect
In pigs, however not significant, there was a continuing increase in plasma-TRX after femur fracture and sequential hemorrhage despite near normalisation of cardiac index and lactate levels.
single-marker and haplotype analyses revealed significant effects of TXNIP (Montrer TXNIP Anticorps) on hot carcass weight, test daily gain, and lifetime daily gain
Crystallization and X-ray crystallographic analysis of recombinant Trx1 has been reported.
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 (Montrer ZAP70 Anticorps)) 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
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.
, ATL-derived factor
, TXN delta 3
, surface-associated sulphydryl protein
, thioredoxin delta 3
, thioredoxin-like protein