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Human Monoclonal TXN Primary Antibody für 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. in The Journal of experimental medicine 1999
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Human Polyclonal TXN Primary Antibody für 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. in Developmental and comparative immunology 2013
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Human Monoclonal TXN Primary Antibody für IHC (fro), IHC (p) - ABIN2476763
Poole, Morgan, Bebbington: Analysis of ecdysones by gas chromatography using electron capture detection. in Journal of chromatography 1975
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Human Monoclonal TXN Primary Antibody für IHC (fro), IHC (p) - ABIN151171
Perkins, Di Trapani, McKay, Clarke: Immunocytochemical localization of thioredoxin in human trophoblast and decidua. in Placenta 1996
Human Monoclonal TXN Primary Antibody für 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. in 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 (zeige VAC14 Antikörper) 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 (zeige MLL Antikörper) expression is associated with myocardial infarction.
Data show that suberoylanilide hydroxamic acid (SAHA) induced apoptosis via the down-regulation thioredoxin1 (Trx1 (zeige MLL Antikörper)), which was regulated by microRNA miR (zeige MLXIP Antikörper)-129-5p.
Analysis of 25 independent cohorts with 5910 patients showed that Trx1 (zeige MLL Antikörper) and TrxR1 (zeige TXNRD1 Antikörper) 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 (zeige MLL Antikörper) and APEX1 (zeige APEX1 Antikörper) expressions are up regulated in new Multiple Sclerosis (MS) patients compared to controls and might be implicated in pathogenesis of the disease.
CD40 (zeige CD40 Antikörper) activation resulted in down-regulation of Thioredoxin (Trx)-1 to permit ASK1 (zeige MAP3K5 Antikörper) activation and apoptosis. Although soluble receptor (zeige IFNAR1 Antikörper) agonist alone could not induce death, combinatorial treatment incorporating soluble CD40 (zeige CD40 Antikörper) agonist and pharmacological inhibition of Trx-1 (zeige MLL Antikörper) was functionally equivalent to the signal triggered by mCD40L
our findings identify the TXN-FOXO1 (zeige FOXO1 Antikörper)-p300 (zeige EP300 Antikörper) circuit as the sensor and effector of oxidative stress in DLBCL cells
Novel positive feedback loop between Trx-1 (zeige MLL Antikörper) and S100P (zeige S100P Antikörper) promotes colorectal cancer invasion and metastasis.
A novel mouse model for the identification of thioredoxin-1 protein interactions has been created.
Serum thioredoxin reductase (zeige PRDX2 Antikörper) is highly increased in mice with hepatocellular carcinoma and its activity is restrained by several mechanisms, in particular, by the serum QSOX1 (zeige QSOX1 Antikörper).
Nuclear overexpression of Trx1 restored Nrf2 (zeige NFE2L2 Antikörper) 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 (zeige GSR Antikörper) is not essential for the maintenance of antioxidant defenses in mouse cochlea; the thioredoxin/thioredoxin reductase (zeige PRDX2 Antikörper) system can probably operate as a functional backup for GSR (zeige GSR Antikörper).
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 (zeige DNAJC5 Antikörper)(370)-Cys (zeige DNAJC5 Antikörper)(371) disulfide bond of TG2 (zeige TGM2 Antikörper) as one of clearest examples of an allosteric disulfide bond in mammals.
Thioredoxin-mediated deglutathionylation of eNOS (zeige NOS3 Antikörper) 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 (zeige CREB1 Antikörper).
results suggest that PostC prevents Trx-1 degradation, decreasing oxidative stress and allowing the activation of Akt (zeige AKT1 Antikörper) and GSK3beta (zeige GSK3b Antikörper) 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 (zeige TXNIP Antikörper) 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 (zeige ZAP70 Antikörper)) 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